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rabbit anti ampkα polyclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti ampkα polyclonal antibody
    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an <t>AMPK</t> agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.
    Rabbit Anti Ampkα Polyclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 3862 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier"

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    Journal: Neural Regeneration Research

    doi: 10.4103/NRR.NRR-D-23-01511

    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.
    Figure Legend Snippet: Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

    Techniques Used: Control, Expressing, Western Blot, Immunofluorescence, Staining, Tandem Mass Spectroscopy

    The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.
    Figure Legend Snippet: The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.

    Techniques Used: Protein-Protein interactions, Expressing, RNA Sequencing, Control, Binding Assay, Real-time Polymerase Chain Reaction

    Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.
    Figure Legend Snippet: Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.

    Techniques Used: Western Blot, Expressing, Control, Phospho-proteomics, Real-time Polymerase Chain Reaction

    Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.
    Figure Legend Snippet: Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

    Techniques Used: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Phospho-proteomics, Real-time Polymerase Chain Reaction



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    AYN activated <t>AMPKα</t> pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity <t>for</t> <t>GLUT4/β‐Actin,</t> CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).
    Anti Ampkα 164, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti ampkα polyclonal antibody  (Cell Signaling Technology Inc)
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    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an <t>AMPK</t> agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.
    Rabbit Anti Ampkα Polyclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti phospho ampkα monoclonal antibody  (Cell Signaling Technology Inc)
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    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an <t>AMPK</t> agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.
    Rabbit Anti Phospho Ampkα Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

    Journal: Research

    Article Title: A Novel Autophagy Inhibitor p -Hydroxylcinnamaldehyde Suppresses Esophageal Squamous Cell Carcinoma by Targeting LDHA Phosphorylation-Mediated Metabolic Reprogramming

    doi: 10.34133/research.1070

    Figure Lengend Snippet: CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

    Article Snippet: Antibodies against actin (20536-1-AP), LC3B (14600-1-AP), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (10494-1-AP), p-mTOR (67778-1-Ig), mTOR (66888-1-Ig), AMPK (66536-1-Ig), P70S6K (14485-1-AP), and ULK1 (20986-1-AP) were purchased from Proteintech Group (Wuhan, China).

    Techniques: Activity Assay, Western Blot, Concentration Assay, Control

    AYN activated AMPKα pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).

    Journal: Food Science & Nutrition

    Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

    doi: 10.1002/fsn3.71429

    Figure Lengend Snippet: AYN activated AMPKα pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).

    Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

    Techniques: Expressing, Muscles, Control

    AYN increased glucose uptake of 3T3‐L1 adipocytes by activating AMPKα/GLUT4 pathway. (A) AYN increased GLUT4 and p‐AMPKα expression in 3T3‐L1 adipocytes; (B) Relative band intensity for GLUT4/β‐Actin, p‐AMPKα/AMPKα for protein in 3T3‐L1 adipocytes; (C) AYN increased the glucose uptake of 3T3‐L1 adipocytes; (D) AMPKα inhibitor, Compound C, suppressed the GLUT4 expression of 3T3‐L1 adipocytes induced by AYN; (E) Compound C inhibited the glucose uptake of 3T3‐L1 adipocytes induced by AYN. ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Normal control group; +++ p < 0.001, compared with AYN group in E).

    Journal: Food Science & Nutrition

    Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

    doi: 10.1002/fsn3.71429

    Figure Lengend Snippet: AYN increased glucose uptake of 3T3‐L1 adipocytes by activating AMPKα/GLUT4 pathway. (A) AYN increased GLUT4 and p‐AMPKα expression in 3T3‐L1 adipocytes; (B) Relative band intensity for GLUT4/β‐Actin, p‐AMPKα/AMPKα for protein in 3T3‐L1 adipocytes; (C) AYN increased the glucose uptake of 3T3‐L1 adipocytes; (D) AMPKα inhibitor, Compound C, suppressed the GLUT4 expression of 3T3‐L1 adipocytes induced by AYN; (E) Compound C inhibited the glucose uptake of 3T3‐L1 adipocytes induced by AYN. ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Normal control group; +++ p < 0.001, compared with AYN group in E).

    Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

    Techniques: Expressing, Control

    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Control, Expressing, Western Blot, Immunofluorescence, Staining, Tandem Mass Spectroscopy

    The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Protein-Protein interactions, Expressing, RNA Sequencing, Control, Binding Assay, Real-time Polymerase Chain Reaction

    Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Western Blot, Expressing, Control, Phospho-proteomics, Real-time Polymerase Chain Reaction

    Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Phospho-proteomics, Real-time Polymerase Chain Reaction

    Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Chitosan alleviates motor dysfunction and improves DA neuron survival in an MPTP-induced mouse model of PD. (A) Experimental timeline of behavioral tests and sample collection from the different treatment groups, including control, NaA alone, MPTP-induced PD model, MPTP + NaA, chitosan treatment, MPTP + chitosan + PPARD antagonist, and SCFA treatment. (B) Experimental timeline of cell treatment with acetate, an AMPK agonist, and a PPARD agonist. (C) Chitosan significantly increased mouse body weight ( n = 7/group). (D) In the rotarod test, fall latency was increased after chitosan treatment ( n = 7/group). (E) Chitosan administration significantly increased TH expression, as determined by western blot assay. GAPDH was used as loading control ( n = 3/group). (F) Chitosan treatment significantly increased the number of TH-positive dopaminergic neurons (red, Alexa Fluor 594), as determined by immunofluorescence staining ( n = 3/group). Scale bars: 100 μm. (G) UHPLC-MS/MS was used to detect DA, DOPAC, and HVA levels in striatum tissue ( n = 4/group). Treatment with chitosan significantly upregulated the levels of DA, DOPAC/DA, and (DOPAC + HVA)/DA, but there was no significant change in HVA/DA levels. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (two-way analysis of variance followed by Tukey’s multiple comparisons test (C) or one-way analysis of variance followed by Tukey’s multiple comparisons test (D–G). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DA: dopamine; DOPAC: 3,4-dihydroxyphenylacetic acid; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HVA: homovanillic acid; ig: intragastrical administration; ip: intraperitoneal administration; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: no significance; NaA: sodium acetate; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; SCFA: short-chain fatty acid; SN: substantia nigra; TH: tyrosine hydroxylase.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Control, Expressing, Western Blot, Immunofluorescence, Staining, Tandem Mass Spectroscopy

    The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: The PPAR and AMPK signaling pathways are enriched in genes whose expression is altered by acetate supplementation, as determined by RNA sequencing of colon tissue from a mouse model of PD. (A) Venn diagram of DEGs among three datasets. (B) KEGG pathway enrichment analysis showed that these DEGs were enriched in the PPAR and AMPK signaling pathways, which are associated with inflammation. (C) Heatmap analysis of 183 common DEGs between MPTP vs . MPTP + Chitosan and MPTP + Chitosan vs . MPTP + Chitosan + NaA ( n = 2/group). (D) qPCR verification analysis of the mRNA levels (normalized to the control group) of the PPAR and AMPK signaling pathway–related genes whose expression was altered in mouse colon tissue ( n = 3/group). All data are presented as the mean ± SD. All experiments were repeated three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DEGs: differentially expressed genes; FABP5: fatty acid-binding protein 5; FASN: fatty acid synthase; KEGG: Kyoto Encyclopedia of Genes and Genomes; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; n.s.: not significant; NaA: sodium acetate; PD: Parkinson’s disease; PPAR: peroxisome proliferators-activated receptor; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; SCD1: stearoyl-coenzyme A desaturase 1; SCD4: stearoyl-coenzyme A desaturase 4.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Protein-Protein interactions, Expressing, RNA Sequencing, Control, Binding Assay, Real-time Polymerase Chain Reaction

    Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Acetate may relieve inflammation by activating the PPARD/AMPK signaling pathway in Caco-2 cells. (A, B) Western blot analysis of PPARD, p-AMPK, and AMPK expression in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, PPARD and p-AMPK expression levels were significantly increased in the group treated with acetate and the PPARD agonist. (C) qPCR was used to detect the mRNA level of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with a PPARD agonist or left untreated. Compared with the acetate group, IL-1β and TNF-α were down-regulated, and iNOS was up-regulated, in cells treated with the PPARD agonist. (D, E) Western blot analysis of AMPK, p-AMPK, and PPARD expression levels in Caco-2 cells treated with an AMPK agonist or left untreated. p-AMPK expression was significantly lower in the group treated with acetate and an AMPK agonist than in the acetate-only group. PPARD expression was not altered by treatment with the AMPK agonist. (F) qPCR was used to detect the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in Caco-2 cells treated with the AMPK agonist or left untreated. Treatment with the AMPK agonist reduced IL-1β, iNOS, IL-6, and TNF-α expression levels compared with treatment with acetate alone. GAPDH was used as loading control in the western blot assays. All data (normalized by control group) are presented as the mean ± SD ( n = 3/group). All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test). AMPK: Adenosine 5′-monophosphate-activated protein kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: no significance; p-AMPK: phosphorylation adenosine 5’-monophosphate-activated protein kinase; PPARD: peroxisome proliferator-activated receptor delta; qPCR: quantitative polymerase chain reaction; TNF-α: tumor necrosis factor alpha.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Western Blot, Expressing, Control, Phospho-proteomics, Real-time Polymerase Chain Reaction

    Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

    Journal: Neural Regeneration Research

    Article Title: Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood–brain barrier

    doi: 10.4103/NRR.NRR-D-23-01511

    Figure Lengend Snippet: Chitosan may reduce acetate levels, thereby activating the PPARD-AMPK signaling pathway, which promotes repair of the intestinal barrier and reduces neuroinflammation in an MPTP-induced mouse model of PD. (A, B) Western blot analysis of p-AMPK, AMPK, and PPARD levels in mouse colon tissue ( n = 3/group). Treatment with acetate significantly increased p-AMPK and PPARD expression. (C) Treatment with a PPARD antagonist significantly decreased mouse body weight ( n = 6/group). (D) There were no significant differences in fall latency among the groups in the rotarod test, which was used to assess motor dysfunction ( n = 6/group). (E–G) PPARD antagonist treatment significantly decreased PPARD, TH, ZO-1, and occludin expression, as determined by western blot ( n = 3/group). (H) Immunofluorescence staining for ZO-1 (green, Alexa Fluor 488) and occludin (red, Alexa Fluor 594) in mouse colon tissue ( n = 3/group). The PPARD antagonist treatment group exhibited markedly reduced ZO-1 and occludin mRNA expression levels in colon tissue. Scale bars: 10 μm. (I) QPCR was used to measure the mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in mouse colon tissue ( n = 3/group). Treatment with the PPARD antagonist increased IL-6 and TNF-α mRNA levels, while IL-8 and iNOS levels were reduced. (J) ELISA was used to detect IL-1β, IL-6, IL-10, and TNF-α expression levels in mouse plasma ( n = 5/group). IL-1β, IL-6, and TNF-α expression levels were significantly increased in the PPARD antagonist treatment group. (K) QPCR was used to measure mRNA levels of IL-1β, IL-6, IL-8, IL-10, TNF-α, and iNOS in the SN ( n = 3/group). Treatment with the PPARD antagonist significantly increased the mRNA levels of IL-1β, IL-6, and IL-8. (L) Treatment with the PPARD antagonist reduced p-AMPK, but not AMPK, expression ( n = 3/group). GAPDH was used as the internal reference. All data are presented as the mean ± SD. All experiments were repeated at least three times. * P < 0.05 (one-way analysis of variance followed by Tukey’s multiple comparisons test (A, B) or unpaired t -test (C–L)). AMPK: Adenosine 5′-monophosphate-activated protein kinase; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL-1β: interleukin-1 Beta; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; iNOS: inductible nitric oxide synthase; n.s.: not significant; NaA: sodium acetate; p-AMPK: phosphorylation adenosine 5′-monophosphate-activated protein kinase; PD: Parkinson’s disease; PPARD: peroxisome proliferator-activated receptor delta; QPCR: quantitative polymerase chain reaction; SN: substantia nigra; TH: tyrosine hydroxylase; TNF-α: tumor necrosis factor alpha; ZO-1: Zonula occludens-1.

    Article Snippet: The primary antibodies used were as follows: rabbit anti-glyceraldehyde-3-phosphate dehydrogenase polyclonal antibody (GAPDH; 1:10,000, Proteintech, Wuhan, Hubei, China, Cat# 10494-1-AP, RRID: AB_2263076), rabbit anti-TH polyclonal antibody (1:5000, Proteintech, Cat# 25859-1-AP, RRID: AB_2716568), rabbit anti-zonula occludens-1 polyclonal antibody (ZO-1; 1:5000, Proteintech, Cat# 21773-1-AP, RRID: AB_10733242), rabbit anti-occludin polyclonal antibody (1:15,000, Proteintech, Cat# 27260-1-AP, RRID: AB_2880820), rabbit anti-AMPKα polyclonal antibody (1:1000, Cell Signaling Technology, Danvers, Massachusetts, USA, Cat# 2532, RRID: AB_330331), rabbit anti-phospho-AMPKα monoclonal antibody (1:1000, Cell Signaling Technology, Cat# 2535, RRID: AB_331250), and rabbit anti-PPARD polyclonal antibody (1:1000, Abcam, Cambridge, UK, Cat# ab23673, RRID: AB_2165902).

    Techniques: Western Blot, Expressing, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Phospho-proteomics, Real-time Polymerase Chain Reaction