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p p38  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p p38
    P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 29927 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+p38/pmc13019078-153-12-23?v=Cell+Signaling+Technology+Inc
    Average 99 stars, based on 29927 article reviews
    p p38 - by Bioz Stars, 2026-08
    99/100 stars

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    Effects of OST on cardiac autophagy and the <t>p38MAPK/mTOR</t> signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.
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    Effects of OST on cardiac autophagy and the <t>p38MAPK/mTOR</t> signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.
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    The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, <t>p38,</t> PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.
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    Effect of Lut on 42 °C-stressed differential gene and protein expression in cells by transcriptomic analysis and western blot, respectively. (A) A volcano plot illustrating differentially regulated gene expression between HS and HS + Lut (10 μM). Genes upregulated and downregulated are shown in red and blue, respectively. (B) Top 20 of GO enrichment about molecular function. (C) Top 20 of GO enrichment about biological process. (D) Top 20 of KEGG enrichment. The color and size of the bubbles represented the significance of the processes and the number of genes, respectively. (E, F) Effect of Lut (10 μM) on total <t>p-p38,</t> p38, Hsp70, and Hsp90 protein expression. β-actin was used as an internal control for proteins. n = 3. Data are expressed as mean ± SD. * represents the significant difference compared with the control group ( P < 0.05), # represents the significant difference compared with the HS ( P < 0.05).
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    Cell Signaling Technology Inc p p38 4511s antibodies
    YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and <t>p38</t> signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.
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    Proteintech p p38 mapk polyclonal antibody
    Itaconate Regulates Lysosomal Function, Calcium Signaling, and <t>p38</t> MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification <t>of</t> <t>p-p38</t> and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.
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    Cell Signaling Technology Inc p p38 mapk
    MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of <t>p-p38</t> and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.
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    Huabio Inc p p38
    MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of <t>p-p38</t> and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.
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    Image Search Results


    Effects of OST on cardiac autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.

    Journal: Journal of Traditional and Complementary Medicine

    Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

    doi: 10.1016/j.jtcme.2025.06.001

    Figure Lengend Snippet: Effects of OST on cardiac autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-p38MAPK, p38MAPK, p-mTOR and mTOR. (H) Quantitative analysis of p-p38MAPK/p38MAPK and p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group.

    Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

    Techniques: Transmission Assay, Electron Microscopy, Western Blot

    Effects of OST on autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice after SB203580 administration. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-mTOR and mTOR. (H) Quantitative analysis of p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). # P < 0.05, ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group; ▲ P < 0.05, ▲▲ P < 0.01 vs the TRZ + OST H group.

    Journal: Journal of Traditional and Complementary Medicine

    Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

    doi: 10.1016/j.jtcme.2025.06.001

    Figure Lengend Snippet: Effects of OST on autophagy and the p38MAPK/mTOR signaling pathway in TRZ-treated mice after SB203580 administration. (A–B) Representative images of transmission electron microscopy images, yellow arrow, mitochondria; red arrow, autophagosome. (C) Representative western blotting bands for LC3I, LC3II, Beclin-1, p62. (D–F) Quantitative analysis of LC3II/I, Beclin-1, p62 (normalized to GAPDH). (G) Representative western blotting bands for p-mTOR and mTOR. (H) Quantitative analysis of p-mTOR/mTOR. Data are expressed as means ± SEM ( n = 3). # P < 0.05, ## P < 0.01 vs the CON group; ∗ P < 0.05, ∗∗ P < 0.01 vs the TRZ group; ▲ P < 0.05, ▲▲ P < 0.01 vs the TRZ + OST H group.

    Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

    Techniques: Transmission Assay, Electron Microscopy, Western Blot

    Schematic illustration summarizing the protective effects of OST against TRZ-induced cardiotoxicity by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.

    Journal: Journal of Traditional and Complementary Medicine

    Article Title: Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway

    doi: 10.1016/j.jtcme.2025.06.001

    Figure Lengend Snippet: Schematic illustration summarizing the protective effects of OST against TRZ-induced cardiotoxicity by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.

    Article Snippet: The first antibodies to Bax (1:1000 dilution, A0207), Bcl-2 (1:800 dilution, A0208), Caspase-3 (1:800 dilution, A2156), LC3 (1:500 dilution, A19665), Beclin-1 (1:1000 dilution, A7353), p62 (1:1000 dilution, A19700) and GAPDH (1:800 dilution, A19056) were purchased from ABclonal Company (Wuhan, China), p38MAPK (1:1000 dilution, bs-0637R) and p-p38MAPK (1:1000 dilution, bs-0636R) were purchased from Bioss Company (Beijing, China), mTOR (1:1000 dilution, #2983) and p-mTOR (1:1000 dilution, #2971) were purchased from CST Company (Danvers, MA, USA).

    Techniques:

    The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

    Journal: Poultry Science

    Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

    doi: 10.1016/j.psj.2026.106922

    Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

    Article Snippet: p-p38 MAPK Rabbit Ab , Abmart , TA4001 , 1: 1500.

    Techniques: Expressing

    The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

    Journal: Poultry Science

    Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

    doi: 10.1016/j.psj.2026.106922

    Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

    Article Snippet: p-p38 MAPK Rabbit Ab , Abmart , TA4001 , 1: 1500.

    Techniques: Activity Assay

    Effect of Lut on 42 °C-stressed differential gene and protein expression in cells by transcriptomic analysis and western blot, respectively. (A) A volcano plot illustrating differentially regulated gene expression between HS and HS + Lut (10 μM). Genes upregulated and downregulated are shown in red and blue, respectively. (B) Top 20 of GO enrichment about molecular function. (C) Top 20 of GO enrichment about biological process. (D) Top 20 of KEGG enrichment. The color and size of the bubbles represented the significance of the processes and the number of genes, respectively. (E, F) Effect of Lut (10 μM) on total p-p38, p38, Hsp70, and Hsp90 protein expression. β-actin was used as an internal control for proteins. n = 3. Data are expressed as mean ± SD. * represents the significant difference compared with the control group ( P < 0.05), # represents the significant difference compared with the HS ( P < 0.05).

    Journal: Poultry Science

    Article Title: Targeted intestinal delivery of luteolin microcapsules as a precision nutritional strategy to alleviate heat stress and enhance growth performance in broilers

    doi: 10.1016/j.psj.2026.106976

    Figure Lengend Snippet: Effect of Lut on 42 °C-stressed differential gene and protein expression in cells by transcriptomic analysis and western blot, respectively. (A) A volcano plot illustrating differentially regulated gene expression between HS and HS + Lut (10 μM). Genes upregulated and downregulated are shown in red and blue, respectively. (B) Top 20 of GO enrichment about molecular function. (C) Top 20 of GO enrichment about biological process. (D) Top 20 of KEGG enrichment. The color and size of the bubbles represented the significance of the processes and the number of genes, respectively. (E, F) Effect of Lut (10 μM) on total p-p38, p38, Hsp70, and Hsp90 protein expression. β-actin was used as an internal control for proteins. n = 3. Data are expressed as mean ± SD. * represents the significant difference compared with the control group ( P < 0.05), # represents the significant difference compared with the HS ( P < 0.05).

    Article Snippet: Anti-HSP90 antibody and Anti-p-p38 antibody were obtained from Cohesion Biosciences Co., Ltd. (England).

    Techniques: Expressing, Western Blot, Gene Expression, Control

    Microcapsule inhibits HS-induced protein expression of p-p38/p38, Hsp70, and Hsp90 in the liver. (A) Effect of microcapsule on total p-p38, p38, Hsp70, and Hsp90 protein expression in liver. (B) Analysis of protein abundance. β-actin was used as an internal control for proteins, n = 3. Data are expressed as mean ± SD. * represents the significant difference compared with the HS group ( P < 0.05). ** represents the highly significant difference compared with the HS group ( P < 0.01). No symbol represents no difference compared with the HS group ( P > 0.05).

    Journal: Poultry Science

    Article Title: Targeted intestinal delivery of luteolin microcapsules as a precision nutritional strategy to alleviate heat stress and enhance growth performance in broilers

    doi: 10.1016/j.psj.2026.106976

    Figure Lengend Snippet: Microcapsule inhibits HS-induced protein expression of p-p38/p38, Hsp70, and Hsp90 in the liver. (A) Effect of microcapsule on total p-p38, p38, Hsp70, and Hsp90 protein expression in liver. (B) Analysis of protein abundance. β-actin was used as an internal control for proteins, n = 3. Data are expressed as mean ± SD. * represents the significant difference compared with the HS group ( P < 0.05). ** represents the highly significant difference compared with the HS group ( P < 0.01). No symbol represents no difference compared with the HS group ( P > 0.05).

    Article Snippet: Anti-HSP90 antibody and Anti-p-p38 antibody were obtained from Cohesion Biosciences Co., Ltd. (England).

    Techniques: Expressing, Quantitative Proteomics, Control

    YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

    Article Snippet: Cyclin B (#4138), Vimentin (#5741), N-cadherin (#13116), p38 (#9212), and p-p38 (#4511S) antibodies were purchased from Cell Signaling Technology (USA).

    Techniques: Protein-Protein interactions, Gene Expression, Control, Western Blot, Migration, Staining, Membrane, Standard Deviation

    YHD inhibits the growth of OS in vivo . (A) The effect of YHD on tumorigenesis in nude mice. (B) The effect of YHD on tumor volume. (C) The effect of YHD on mouse weight. (D) Hematoxylin-eosin staining of the mouse tumor tissue. (E) Hematoxylin-eosin staining of the mouse lung tissue. (F) PCNA, Bcl-2, Vimentin, p-AKT, and p-P38 of the mouse tumor tissue were detected by immunohistochemistry. (G) Hematoxylin-eosin staining of the mouse heart and liver tissue. Data were presented as mean ± standard deviation ( n = 6).

    Journal: Genes & Diseases

    Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

    doi: 10.1016/j.gendis.2025.101862

    Figure Lengend Snippet: YHD inhibits the growth of OS in vivo . (A) The effect of YHD on tumorigenesis in nude mice. (B) The effect of YHD on tumor volume. (C) The effect of YHD on mouse weight. (D) Hematoxylin-eosin staining of the mouse tumor tissue. (E) Hematoxylin-eosin staining of the mouse lung tissue. (F) PCNA, Bcl-2, Vimentin, p-AKT, and p-P38 of the mouse tumor tissue were detected by immunohistochemistry. (G) Hematoxylin-eosin staining of the mouse heart and liver tissue. Data were presented as mean ± standard deviation ( n = 6).

    Article Snippet: Cyclin B (#4138), Vimentin (#5741), N-cadherin (#13116), p38 (#9212), and p-p38 (#4511S) antibodies were purchased from Cell Signaling Technology (USA).

    Techniques: In Vivo, Staining, Immunohistochemistry, Standard Deviation

    Itaconate Regulates Lysosomal Function, Calcium Signaling, and p38 MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification of p-p38 and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.

    Journal: Redox Biology

    Article Title: Stromal cell-derived itaconate promotes endometriosis via macrophage NRF2 and lysosomal pH modulation

    doi: 10.1016/j.redox.2026.104101

    Figure Lengend Snippet: Itaconate Regulates Lysosomal Function, Calcium Signaling, and p38 MAPK Pathway in Macrophages (A) Lysosomal acidification in ascites-derived macrophages from non-endometriosis (NC) and endometriosis (EM) patients assessed by LysoSensor fluorescence intensity (n = 6/group). (B) Lysosomal acidification in PBMC-derived macrophages after LPS,IL-4 and 4-OI treatment (n = 3/group). (C) Lysosomal pH value of BMDMs after LPS and 4-OI treatment (n = 3/group). (D, E) Effect of chloroquine (CQ) on LysoSensor intensity (D) and proportion of iNOS + BMDMs (E) after LPS and 4-OI treatment (n = 3/group). (F) mRNA levels of Il1b , Il6 , Nos2 , and Tnf in BMDMs under indicated treatments (n = 3/group). (G) Intracellular Ca 2+ dynamics in BMDMs after treatments, measured by Fluo-4. (H) Intracellular Ca 2+ dynamics in ascites-derived macrophages from NC and EM patients. (I) Quantification of intracellular calcium in peritoneal macrophages from NC and EM patients (n = 3/group). (J) Quantification of intracellular calcium in BMDMs (n = 5/group). (K) mRNA expression of lysosomal calcium channel genes ( MCOLN1 , MCOLN2 , TPC1 , TPC2 ) in ascites-derived macrophages from NC and EM patients (n = 3/group). (L) lysosomal calcium channel genes mRNA in PBMC-derived macrophages co-cultured with normal ESCs (Nor-ESC), eutopic ESCs (Eu-ESC), or ectopic ESCs (Ec-ESC) from patients (n = 5/group). (M − N) Fluo-4-based Ca 2+ dynamics in BMDMs treated with LPS, 4-OI, ML-SA1 (M), or CQ (N). (O) Flow cytometry analysis and quantification of iNOS + BMDMs after indicated treatments (n = 3/group). (P) mRNA levels of pro-inflammatory genes in BMDMs under different treatments (n = 3/group). (Q) Western blot and quantification of p-p38 and total p38 in BMDMs with LPS ± 4-OI (n = 3/group). (R–S) Western blot and quantification of iNOS, p-p38, and total p38 in BMDMs treated with LPS, 4-OI, and CQ (R), or ML-SA1 (S) (n = 3/group). (Data are presented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.) EM, endometriosis; NC, non-EM control; LPS, lipopolysaccharide; 4-OI, 4-octyl itaconate; CQ, chloroquine; ML-SA1, MCOLN channel agonist; PBMC, peripheral blood mononuclear cell; ESC, endometrial stromal cell.

    Article Snippet: After blocking in 5% milk in TBST, membranes were incubated overnight at 4 °C with primary antibodies: Beta Actin Monoclonal antibody(1:20000, 66009-1-Ig; Proteintech), Beta Tubulin Recombinant antibody (1:5000, 80713-1-RR; Proteintech), Anti-IRG1 antibody (1:1000; ab222411; abcam; Cambridge, UK), Nrf2 monoclonal antibody (1:2000; A21176; abclonal; Wuhan, China), iNOS Polyclonal antibody (1:500; 22226-1-AP; Proteintech), NOX2 Polyclonal antibody (1:3000; 19013-1-AP; Proteintech), p-p38 MAPK Polyclonal antibody (1:2000; 28796-1-AP; Proteintech), and p38 MAPK Polyclonal antibody (1:4000; 14064-1-AP; Proteintech).

    Techniques: Derivative Assay, Fluorescence, Expressing, Cell Culture, Flow Cytometry, Western Blot, Control

    MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of p-p38 and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.

    Journal: Oncology Letters

    Article Title: Schisandrin B suppresses cholangiocarcinoma by targeting the ROS/p38 MAPK/NF-κB axis

    doi: 10.3892/ol.2026.15551

    Figure Lengend Snippet: MAPK signaling pathway inhibition by Sch B. (A) A double luciferase assay analysis of the expression of AP-1 in CCA cells treated with different concentrations of Sch B (from 0 to 160 µmol/l). (B) To evaluate the activity of CCA cells, they were separately treated with Sch B and the MAPK-specific inhibitor SB203580. (C) Western blot analysis of the expression levels of p-p38 and p38. (D) Colony formation assay of CCA cells treated with 160 µmol/l Sch B and 0.5 µmol/l SB203580. Statistical analysis was performed using ANOVA and Dunnett's post hoc test. ***P<0.001. Sch B, Schisandrin B; P, phosphorylated.

    Article Snippet: p-p38 MAPK (Thr180/Tyr182) , 4511 , 1:1,000 , Cell Signaling Technology, Inc..

    Techniques: Inhibition, Luciferase, Expressing, Activity Assay, Western Blot, Colony Assay