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anti il 1β  (Proteintech)


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    Structured Review

    Proteintech anti il 1β
    Anti Il 1β, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2098 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 2098 article reviews
    anti il 1β - by Bioz Stars, 2026-04
    96/100 stars

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    In vivo chondrogenesis of hydrogels incorporated with different combinations of PSF and KSF. (a) Alcian blue and Safranin O staining of different combinations after 21-day implantation. G1: 5 % β-sheet PSF +5 % β-sheet KSF; G2: 15 % β-sheet PSF +30 % β-sheet KSF; G3: 30 % β-sheet PSF +40 % β-sheet KSF; G4: 40 % β-sheet PSF +50 % β-sheet KSF. Scale bar = 200 μm. (b–d) Quantitative analysis of <t>IL-1β,</t> IL-6 and TNF-α surrounding defect cartilage 1 week and 3 weeks after operation. (e, f) Macroscopic and MRI observations of rat femoral condyles at week 6 and 12. Red circles and red arrows show the original defect zone under macroscope and MRI respectively. Scale bar = 1 mm. (g) Relative ratio of average optical density (versus G1) that shows the staining intensity of Alcian blue and Safranin O staining. (h) ICRS scoring of macroscopic evaluations. (i) The repaired cartilage using a nanoindentation instrument. Scale bar = 1 cm. (j, k) Reduced modulus and hardness of the regenerated cartilage. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001.
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    Hippocampal SIRT6 Expression Profile in a Lipopolysaccharide (LPS)-Induced Depression Model. (A) Western blot analysis of SIRT6 expression in the hippocampal brain tissues. D, day. n = 4 mice. (B) Immunostaining for SIRT6 in the hippocampal region three days post-LPS injection revealed an overall reduction in brain tissues, while its expression was concurrently increased specifically in microglia. This was quantified in two graphs showing total SIRT6 expression (left) and microglial SIRT6 expression (right), with arrowheads indicating SIRT6 localization in microglia. n = 4 mice. (C) Western blot analysis of SIRT6 expression in microglia sorted from the hippocampus by MCAS at 3 days post-LPS injection. n = 4 mice. Data are presented as mean ± SEM. Statistical analysis: One-way ANOVA with Tukey's post hoc test in A; Unpaired t -test for two-group comparisons in B-C.
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    iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and <t>IL-1β)</t> in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.
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    Boster Bio anti il 1β
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    Elabscience Biotechnology rat il 1β elisa kit
    Prostaglandin dysregulation and inflammatory response in the RPP model (A–C) Uterine PGF 2α (A), PGE 2 (B), and PGF 2α /PGE 2 ratio (C) on days 12 and 24 of RPP modeling ( n = 3). (D) The protein levels of COX-2 in the uterine tissue on days 12 and 24 of RPP modeling ( n = 3). (E–G) The levels <t>of</t> <t>IL-1β</t> (E), IL-6 (F), and TNF-α (G) in the serum on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, one-way ANOVA.
    Rat Il 1β Elisa Kit, supplied by Elabscience Biotechnology, 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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    Image Search Results


    In vivo chondrogenesis of hydrogels incorporated with different combinations of PSF and KSF. (a) Alcian blue and Safranin O staining of different combinations after 21-day implantation. G1: 5 % β-sheet PSF +5 % β-sheet KSF; G2: 15 % β-sheet PSF +30 % β-sheet KSF; G3: 30 % β-sheet PSF +40 % β-sheet KSF; G4: 40 % β-sheet PSF +50 % β-sheet KSF. Scale bar = 200 μm. (b–d) Quantitative analysis of IL-1β, IL-6 and TNF-α surrounding defect cartilage 1 week and 3 weeks after operation. (e, f) Macroscopic and MRI observations of rat femoral condyles at week 6 and 12. Red circles and red arrows show the original defect zone under macroscope and MRI respectively. Scale bar = 1 mm. (g) Relative ratio of average optical density (versus G1) that shows the staining intensity of Alcian blue and Safranin O staining. (h) ICRS scoring of macroscopic evaluations. (i) The repaired cartilage using a nanoindentation instrument. Scale bar = 1 cm. (j, k) Reduced modulus and hardness of the regenerated cartilage. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Precisely regulated physically-crosslinked carriers enable synergetic release of bioactive factors for MSC-mediated cartilage regeneration

    doi: 10.1016/j.bioactmat.2026.01.009

    Figure Lengend Snippet: In vivo chondrogenesis of hydrogels incorporated with different combinations of PSF and KSF. (a) Alcian blue and Safranin O staining of different combinations after 21-day implantation. G1: 5 % β-sheet PSF +5 % β-sheet KSF; G2: 15 % β-sheet PSF +30 % β-sheet KSF; G3: 30 % β-sheet PSF +40 % β-sheet KSF; G4: 40 % β-sheet PSF +50 % β-sheet KSF. Scale bar = 200 μm. (b–d) Quantitative analysis of IL-1β, IL-6 and TNF-α surrounding defect cartilage 1 week and 3 weeks after operation. (e, f) Macroscopic and MRI observations of rat femoral condyles at week 6 and 12. Red circles and red arrows show the original defect zone under macroscope and MRI respectively. Scale bar = 1 mm. (g) Relative ratio of average optical density (versus G1) that shows the staining intensity of Alcian blue and Safranin O staining. (h) ICRS scoring of macroscopic evaluations. (i) The repaired cartilage using a nanoindentation instrument. Scale bar = 1 cm. (j, k) Reduced modulus and hardness of the regenerated cartilage. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001.

    Article Snippet: The suspension was centrifuged at 10,000 rpm for 10 min at 4 °C, and the supernatant was collected, and Elisa assay was performed following the manufacturer's instructions for rat IL-1β, IL-6, and TNF-α ELISA kits (Elabscience, China).

    Techniques: In Vivo, Staining

    Hippocampal SIRT6 Expression Profile in a Lipopolysaccharide (LPS)-Induced Depression Model. (A) Western blot analysis of SIRT6 expression in the hippocampal brain tissues. D, day. n = 4 mice. (B) Immunostaining for SIRT6 in the hippocampal region three days post-LPS injection revealed an overall reduction in brain tissues, while its expression was concurrently increased specifically in microglia. This was quantified in two graphs showing total SIRT6 expression (left) and microglial SIRT6 expression (right), with arrowheads indicating SIRT6 localization in microglia. n = 4 mice. (C) Western blot analysis of SIRT6 expression in microglia sorted from the hippocampus by MCAS at 3 days post-LPS injection. n = 4 mice. Data are presented as mean ± SEM. Statistical analysis: One-way ANOVA with Tukey's post hoc test in A; Unpaired t -test for two-group comparisons in B-C.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: Hippocampal SIRT6 Expression Profile in a Lipopolysaccharide (LPS)-Induced Depression Model. (A) Western blot analysis of SIRT6 expression in the hippocampal brain tissues. D, day. n = 4 mice. (B) Immunostaining for SIRT6 in the hippocampal region three days post-LPS injection revealed an overall reduction in brain tissues, while its expression was concurrently increased specifically in microglia. This was quantified in two graphs showing total SIRT6 expression (left) and microglial SIRT6 expression (right), with arrowheads indicating SIRT6 localization in microglia. n = 4 mice. (C) Western blot analysis of SIRT6 expression in microglia sorted from the hippocampus by MCAS at 3 days post-LPS injection. n = 4 mice. Data are presented as mean ± SEM. Statistical analysis: One-way ANOVA with Tukey's post hoc test in A; Unpaired t -test for two-group comparisons in B-C.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Expressing, Western Blot, Immunostaining, Injection

    SIRT6 deficiency potentiates microglial activation in a LPS-induced depression model. (A) Immunostaining of GFAP and IBA1 in the hippocampus area in Sirt6 MCKO and Sirt6 fl/fl mice at day 5 post-LPS injection. n = 4 mice. (B-G) Quantification of (B) IBA1 + and (C) GFAP + cell counts, along with microglial morphology parameters: (D) number of branches, (E) average branch length, (F) total branch length, and (G) soma area. n = 4 mice. (H) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: SIRT6 deficiency potentiates microglial activation in a LPS-induced depression model. (A) Immunostaining of GFAP and IBA1 in the hippocampus area in Sirt6 MCKO and Sirt6 fl/fl mice at day 5 post-LPS injection. n = 4 mice. (B-G) Quantification of (B) IBA1 + and (C) GFAP + cell counts, along with microglial morphology parameters: (D) number of branches, (E) average branch length, (F) total branch length, and (G) soma area. n = 4 mice. (H) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Activation Assay, Immunostaining, Injection, Two Tailed Test

    Deletion of microglial Sirt6 inhibited the NRF2-HO1 signaling and worsened the peroxidation damage. (A) Gene Ontology (GO) analysis was performed on RNA-Seq data from microglia sorted from Sirt6 MCKO and Sirt6 fl/fl control mice. (B) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. n = 4 mice. (C) Gene Set Enrichment Analysis (GSEA) of RNA-Seq data profiled from microglia sorted from Sirt6 MCKO and Sirt6 fl/fl control mice. (D-E) Analysis of NRF2-HO1 and associated signaling proteins in sorted microglia. Protein levels of NRF2, KEAP1, HO-1, NQO1, NLRP3, Cleaved Caspase-3, and Cleaved IL-1β were assessed by Western blot (D) and quantified (E). n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: Deletion of microglial Sirt6 inhibited the NRF2-HO1 signaling and worsened the peroxidation damage. (A) Gene Ontology (GO) analysis was performed on RNA-Seq data from microglia sorted from Sirt6 MCKO and Sirt6 fl/fl control mice. (B) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. n = 4 mice. (C) Gene Set Enrichment Analysis (GSEA) of RNA-Seq data profiled from microglia sorted from Sirt6 MCKO and Sirt6 fl/fl control mice. (D-E) Analysis of NRF2-HO1 and associated signaling proteins in sorted microglia. Protein levels of NRF2, KEAP1, HO-1, NQO1, NLRP3, Cleaved Caspase-3, and Cleaved IL-1β were assessed by Western blot (D) and quantified (E). n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: RNA Sequencing, Control, Injection, Western Blot, Two Tailed Test

    Knockout of the Nrf2 in microglial aggravated the depression behavior and facilitated the microglial activation. (A) Experimental timeline depicting the sequential administration of tamoxifen and LPS, followed by behavioral assessment. (B) Western blot analysis confirming the successful knockout of Nrf2 in microglial cells of Nrf2 MCKO mice. n = 3 mice. (C-D) Quantification of the duration of immobility in the (C) TST) and (D) FST. n = 8 mice. (E) Levels of TAC, MDA, SOD, and the GSH/GSSG ratio were measured in Nrf2 MCKO and Nrf2 fl/fl mice 3 days after LPS challenge. (F) Immunostaining of GFAP and IBA1 in the hippocampus area of Nrf2 MCKO and Nrf2 fl/fl mice 3 days after LPS injection. (G-L) Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice. (M) qPCR analysis of TNF-α, IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. (N) Western blot analysis was conducted to determine the protein levels of SIRT6 and NRF2 downstream signaling components in primary microglia purified from the mouse hippocampus. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: Knockout of the Nrf2 in microglial aggravated the depression behavior and facilitated the microglial activation. (A) Experimental timeline depicting the sequential administration of tamoxifen and LPS, followed by behavioral assessment. (B) Western blot analysis confirming the successful knockout of Nrf2 in microglial cells of Nrf2 MCKO mice. n = 3 mice. (C-D) Quantification of the duration of immobility in the (C) TST) and (D) FST. n = 8 mice. (E) Levels of TAC, MDA, SOD, and the GSH/GSSG ratio were measured in Nrf2 MCKO and Nrf2 fl/fl mice 3 days after LPS challenge. (F) Immunostaining of GFAP and IBA1 in the hippocampus area of Nrf2 MCKO and Nrf2 fl/fl mice 3 days after LPS injection. (G-L) Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice. (M) qPCR analysis of TNF-α, IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. (N) Western blot analysis was conducted to determine the protein levels of SIRT6 and NRF2 downstream signaling components in primary microglia purified from the mouse hippocampus. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Knock-Out, Activation Assay, Western Blot, Immunostaining, Injection, Purification, Two Tailed Test

    Sirt6 regulated the microglial activation and the depression behavior through Nrf2-HO1 signaling in vivo (A) Experimental timeline of tamoxifen administration, AAV9-Cx3cr1-Nrf2 injection, LPS challenge, and behavioral tests in Sirt6 MCKO mice. (B) Western blot analysis of NRF2 levels after AAV9-Cx3cr1-Nrf2 injection. n = 3 mice. (C-D) Immobility time in TST (C) and FST (D). n = 8 mice. (E) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. n = 4 mice. (F-L) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (F); Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice. (M) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. (N) Western blot analysis of NRF2 downstream signaling component protein levels in microglia sorted from the hippocampus. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: Sirt6 regulated the microglial activation and the depression behavior through Nrf2-HO1 signaling in vivo (A) Experimental timeline of tamoxifen administration, AAV9-Cx3cr1-Nrf2 injection, LPS challenge, and behavioral tests in Sirt6 MCKO mice. (B) Western blot analysis of NRF2 levels after AAV9-Cx3cr1-Nrf2 injection. n = 3 mice. (C-D) Immobility time in TST (C) and FST (D). n = 8 mice. (E) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. n = 4 mice. (F-L) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (F); Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice. (M) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. (N) Western blot analysis of NRF2 downstream signaling component protein levels in microglia sorted from the hippocampus. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Activation Assay, In Vivo, Injection, Western Blot, Immunostaining, Two Tailed Test

    Overexpression of Sirt6 in microglial improved the depression behavior and impeded the microglial activation (A) Experimental timeline depicting tamoxifen administration, followed by tail vein injection of AAV9-Cx3cr1-Sirt6, subsequent LPS challenge, and finally, a series of behavioral tests. (B) Western blot analysis of SIRT6 expression after AAV9-Cx3cr1-Sirt6 injection. n = 3 mice. (C-D) The immobility time was quantified in TST (C) and FST (D). n = 8 mice. (E) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. (F-L) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (F); Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice.(M) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: Overexpression of Sirt6 in microglial improved the depression behavior and impeded the microglial activation (A) Experimental timeline depicting tamoxifen administration, followed by tail vein injection of AAV9-Cx3cr1-Sirt6, subsequent LPS challenge, and finally, a series of behavioral tests. (B) Western blot analysis of SIRT6 expression after AAV9-Cx3cr1-Sirt6 injection. n = 3 mice. (C-D) The immobility time was quantified in TST (C) and FST (D). n = 8 mice. (E) TAC, MDA, SOD, and GSH/GSSG levels at 5 days after LPS injection. (F-L) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (F); Quantification of (G) IBA1 + and (H) GFAP + cell counts, along with microglial morphology parameters: (I) number of branches, (J) average branch length, (K) total branch length, and (L) soma area. n = 4 mice.(M) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Over Expression, Activation Assay, Injection, Western Blot, Expressing, Immunostaining, Two Tailed Test

    UBCS039-mediated SIRT6 activation exerts antidepressant and anti-inflammatory effects (A) Schematic of the experimental timeline for UBCS039 administration, LPS injection, and behavioral testing. (B-C) The immobility time was measured in TST (B) and FST (C). n = 4 mice. (D-G) TAC (D), MDA (E), SOD (F), and GSH/GSSG (G) levels at 5 days after LPS injection. n = 4 mice. (H-I) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (H); Quantification of IBA1 + and GFAP + cell counts, along with microglial morphology parameters: number of branches, average branch length, total branch length, and soma area (I). n = 4 mice. (J) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Journal: Neurobiology of Stress

    Article Title: Microglial SIRT6 confers protection against neuroinflammation-associated depression through NRF2-HO1 signaling

    doi: 10.1016/j.ynstr.2026.100804

    Figure Lengend Snippet: UBCS039-mediated SIRT6 activation exerts antidepressant and anti-inflammatory effects (A) Schematic of the experimental timeline for UBCS039 administration, LPS injection, and behavioral testing. (B-C) The immobility time was measured in TST (B) and FST (C). n = 4 mice. (D-G) TAC (D), MDA (E), SOD (F), and GSH/GSSG (G) levels at 5 days after LPS injection. n = 4 mice. (H-I) Immunostaining of GFAP and IBA1 in the hippocampus area at 5 days after LPS injection (H); Quantification of IBA1 + and GFAP + cell counts, along with microglial morphology parameters: number of branches, average branch length, total branch length, and soma area (I). n = 4 mice. (J) qPCR analysis of TNF-α,IL-6, and IL-1β mRNA levels in the microglial sorted from the hippocampus brain tissue. n = 4 mice. Data are mean ± SEM. Statistical significance between two groups was determined by an unpaired two-tailed Student's t-test.

    Article Snippet: Membranes were blocked with 5% non-fat milk in TBST for 1 h and incubated overnight at 4 °C with primary antibodies: SIRT6 (12486, Cell Signaling Technology), NRF2 (ab62352, Abcam), HO-1 (ab68477, Abcam), NQO1 (ab80588, Abcam), KEAP1 (8047, Cell Signaling Technology), NLRP3 (AG-20B-0014, AdipoGen), cleaved caspase-1 (4199, Cell Signaling Technology), cleaved IL-1β (83186, Cell Signaling Technology), and β-actin (A1978, Sigma-Aldrich).

    Techniques: Activation Assay, Injection, Immunostaining, Two Tailed Test

    Schematic diagram illustrates the mechanism of Mn-NC composite hydrogels for TMJ-OA treatment. Composite hydrogels can effectively protect chondrocytes from ROS damage, alleviate inflammatory reactions within the joint microenvironment, inhibit inflammation-induced chondrocyte apoptosis and ECM degradation, and simultaneously induce the regeneration and repair of subchondral bones via the enzyme-like activity of Mn-NC SAzymes and the release of Mn ions.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: Schematic diagram illustrates the mechanism of Mn-NC composite hydrogels for TMJ-OA treatment. Composite hydrogels can effectively protect chondrocytes from ROS damage, alleviate inflammatory reactions within the joint microenvironment, inhibit inflammation-induced chondrocyte apoptosis and ECM degradation, and simultaneously induce the regeneration and repair of subchondral bones via the enzyme-like activity of Mn-NC SAzymes and the release of Mn ions.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Activity Assay

    Characterization of Mn-NC SAzymes. (a) Preparation of Mn-NC SAzymes. (b) TEM images of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (c) HAADF-STEM image of Mn-NC-10 SAzymes and the corresponding EDX elemental mappings of C, N, O, and Mn. Inset: the SAED pattern. (d) Aberration-corrected HAADF-STEM image of Mn-NC-10 SAzymes. (e) XRD patterns of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (f) Mn 2p and (g) Mn 3s XPS spectra of Mn-NC-10 SAzymes. (h) XANES and (i) FT EXAFS spectra of Mn-NC-10 SAzymes and reference samples at the Mn K-edge. (j) FT EXAFS spectra fitting curves of Mn-NC-10 SAzymes at the Mn K-edge (inset: structure model).

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: Characterization of Mn-NC SAzymes. (a) Preparation of Mn-NC SAzymes. (b) TEM images of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (c) HAADF-STEM image of Mn-NC-10 SAzymes and the corresponding EDX elemental mappings of C, N, O, and Mn. Inset: the SAED pattern. (d) Aberration-corrected HAADF-STEM image of Mn-NC-10 SAzymes. (e) XRD patterns of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (f) Mn 2p and (g) Mn 3s XPS spectra of Mn-NC-10 SAzymes. (h) XANES and (i) FT EXAFS spectra of Mn-NC-10 SAzymes and reference samples at the Mn K-edge. (j) FT EXAFS spectra fitting curves of Mn-NC-10 SAzymes at the Mn K-edge (inset: structure model).

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques:

    SOD/CAT-like activity and DFT calculations of the Mn-NC SAzymes. The SOD-like activity (a), H 2 O 2 scavenging ratio (b), and dissolved O 2 production curves (c) of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (d) •OH scavenging abilities of Mn-NC-10 evaluated by the electron spin resonance (ESR) spectroscopy. (e) Dissolved oxygen generation catalyzed by Mn-NC-10 at pH 6.6 under varying H 2 O 2 concentrations. (f) Michaelis-Menten kinetic curves of Mn-NC-10 derived from dissolved oxygen production by varying H 2 O 2 concentration. (g) Gibbs free-energy step diagram of the Mn-N 4 . (h) Gibbs free energy step diagram of N 4 C and Mn-N 4 -O in the CAT-like catalytic reaction. (i) Schematic of CAT-like catalytic reaction of N 4 C. (j) Schematic of CAT-like catalytic reaction of Mn-N 4 . (k) Differential charge profiles before and after introducing Mn-O to N 4 C. (l) Differential charge of H 2 O and O 2 before and after adsorption to N 4 C and Mn-N 4 -O (yellow represents gain of electrons, blue represents loss of electrons). TEM images (m), Mn ion releasing amount (n), changes of CAT-like activity (o), and changes of SOD-like activity (p) of Mn-NC-10 SAzymes incubated in PBS (pH = 7.0–7.6) for different time.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: SOD/CAT-like activity and DFT calculations of the Mn-NC SAzymes. The SOD-like activity (a), H 2 O 2 scavenging ratio (b), and dissolved O 2 production curves (c) of NC, Mn-NC-1, Mn-NC-5, and Mn-NC-10 SAzymes. (d) •OH scavenging abilities of Mn-NC-10 evaluated by the electron spin resonance (ESR) spectroscopy. (e) Dissolved oxygen generation catalyzed by Mn-NC-10 at pH 6.6 under varying H 2 O 2 concentrations. (f) Michaelis-Menten kinetic curves of Mn-NC-10 derived from dissolved oxygen production by varying H 2 O 2 concentration. (g) Gibbs free-energy step diagram of the Mn-N 4 . (h) Gibbs free energy step diagram of N 4 C and Mn-N 4 -O in the CAT-like catalytic reaction. (i) Schematic of CAT-like catalytic reaction of N 4 C. (j) Schematic of CAT-like catalytic reaction of Mn-N 4 . (k) Differential charge profiles before and after introducing Mn-O to N 4 C. (l) Differential charge of H 2 O and O 2 before and after adsorption to N 4 C and Mn-N 4 -O (yellow represents gain of electrons, blue represents loss of electrons). TEM images (m), Mn ion releasing amount (n), changes of CAT-like activity (o), and changes of SOD-like activity (p) of Mn-NC-10 SAzymes incubated in PBS (pH = 7.0–7.6) for different time.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Activity Assay, Electron Paramagnetic Resonance, Spectroscopy, Derivative Assay, Concentration Assay, Adsorption, Incubation

    The Mn-NC composite hydrogels protect chondrocytes from H 2 O 2 -induced damage by attenuating ROS. (a) Live/dead staining of rat chondrocytes after incubation with different hydrogels for 24 h, scale bar = 200 μm. (b) Cell viability of rat chondrocytes after incubation with different hydrogels for 1, 2, and 3 days. (c) Cell viability, (d) Intracellular ROS content, and (e) Bright-field and ROS staining of rat chondrocytes after incubation with different hydrogels under H 2 O 2 -contaning condition for 24 h, scale bar = 50 μm. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group, #p < 0.05, ##p < 0.01, and ###p < 0.001 suggests a significant difference in comparison to the Control + H 2 O 2 group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The Mn-NC composite hydrogels protect chondrocytes from H 2 O 2 -induced damage by attenuating ROS. (a) Live/dead staining of rat chondrocytes after incubation with different hydrogels for 24 h, scale bar = 200 μm. (b) Cell viability of rat chondrocytes after incubation with different hydrogels for 1, 2, and 3 days. (c) Cell viability, (d) Intracellular ROS content, and (e) Bright-field and ROS staining of rat chondrocytes after incubation with different hydrogels under H 2 O 2 -contaning condition for 24 h, scale bar = 50 μm. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group, #p < 0.05, ##p < 0.01, and ###p < 0.001 suggests a significant difference in comparison to the Control + H 2 O 2 group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Staining, Incubation, Comparison, Control

    The Mn-NC composite hydrogels protect chondrocytes from IL-1β-induced damage and promote subchondral bone remodeling by stimulating osteogenic differentiation of human mesenchymal stem cells. Cell viability (a) and expressions of inflammatory factors TNF-α (b), IL-6 (c), and inflammation-related proteins (d) in chondrocytes after stimulation with IL-1β. The expressions of inflammatory factors including TNF-α (e), iNOS (f), IL-6 (g), IL-1β (h) and corresponding proteins (i) from rat macrophages (NR8383) co-cultured with Control, Control + H 2 O 2 , NAC + H 2 O 2 , CH + H 2 O 2 , CH@Mn2+H 2 O 2 groups. (j) ALP-positive area staining images from Control, CH, and CH@Mn2 groups at 7 days and corresponding quantitative ALP activity. Scale bar = 200 μm. (k) Expression of osteogenesis-related genes and proteins including ALP, BMP2, OPN from Control, CH, and CH@Mn2 groups at 7 days. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group, # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the Control + IL-1β, Control + H 2 O 2 or CH group. ▽ p < 0.05, ▽▽ p < 0.01, and ▽▽▽ p < 0.001 suggests a significant difference in comparison to the NAC + IL-1β or NAC + H 2 O 2 group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The Mn-NC composite hydrogels protect chondrocytes from IL-1β-induced damage and promote subchondral bone remodeling by stimulating osteogenic differentiation of human mesenchymal stem cells. Cell viability (a) and expressions of inflammatory factors TNF-α (b), IL-6 (c), and inflammation-related proteins (d) in chondrocytes after stimulation with IL-1β. The expressions of inflammatory factors including TNF-α (e), iNOS (f), IL-6 (g), IL-1β (h) and corresponding proteins (i) from rat macrophages (NR8383) co-cultured with Control, Control + H 2 O 2 , NAC + H 2 O 2 , CH + H 2 O 2 , CH@Mn2+H 2 O 2 groups. (j) ALP-positive area staining images from Control, CH, and CH@Mn2 groups at 7 days and corresponding quantitative ALP activity. Scale bar = 200 μm. (k) Expression of osteogenesis-related genes and proteins including ALP, BMP2, OPN from Control, CH, and CH@Mn2 groups at 7 days. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group, # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the Control + IL-1β, Control + H 2 O 2 or CH group. ▽ p < 0.05, ▽▽ p < 0.01, and ▽▽▽ p < 0.001 suggests a significant difference in comparison to the NAC + IL-1β or NAC + H 2 O 2 group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Cell Culture, Control, Staining, Activity Assay, Expressing, Comparison

    The Mn-NC composite hydrogels inhibit chondrocyte apoptosis and ECM degradation in rats after IL-1β stimulation. Nucleus, apoptosis, and cytoskeleton staining of chondrocytes (a) and flow cytometry analysis (b) after IL-1β stimulation, scale bar = 50 μm. Expressions of apoptosis-related genes and proteins including Bax and Bcl2 (c) and ECM degeneration related genes and proteins including Adamts5 and MMP13 (d) from Control, Control + IL-1β, NAC + IL-1β, CH + IL-1β, and CH@Mn2+IL-1β groups. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the Control + IL-1β group. ▽ p < 0.05, ▽▽ p < 0.01, and ▽▽▽ p < 0.001 suggests a significant difference in comparison to the NAC + IL-1β group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The Mn-NC composite hydrogels inhibit chondrocyte apoptosis and ECM degradation in rats after IL-1β stimulation. Nucleus, apoptosis, and cytoskeleton staining of chondrocytes (a) and flow cytometry analysis (b) after IL-1β stimulation, scale bar = 50 μm. Expressions of apoptosis-related genes and proteins including Bax and Bcl2 (c) and ECM degeneration related genes and proteins including Adamts5 and MMP13 (d) from Control, Control + IL-1β, NAC + IL-1β, CH + IL-1β, and CH@Mn2+IL-1β groups. Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Control group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the Control + IL-1β group. ▽ p < 0.05, ▽▽ p < 0.01, and ▽▽▽ p < 0.001 suggests a significant difference in comparison to the NAC + IL-1β group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Staining, Flow Cytometry, Control, Comparison

    The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 2 weeks. (a) Schematic diagram of in vivo experiments of hydrogel treatment of TMJ-OA. HE staining (b), SO/FG staining (c), immunohistochemical staining of COLII (d) and MMP13 (e), immunofluorescence staining of CD86 (f) and CD206 (g) at the synovial, and immunofluorescence staining of IL-1β (h) in the TMJ of rats after 2 weeks of treatment, scale bar = 100 μm. (i) Histological OARSI score of articular cartilage after 2 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (c–h). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 2 weeks. (a) Schematic diagram of in vivo experiments of hydrogel treatment of TMJ-OA. HE staining (b), SO/FG staining (c), immunohistochemical staining of COLII (d) and MMP13 (e), immunofluorescence staining of CD86 (f) and CD206 (g) at the synovial, and immunofluorescence staining of IL-1β (h) in the TMJ of rats after 2 weeks of treatment, scale bar = 100 μm. (i) Histological OARSI score of articular cartilage after 2 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (c–h). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: In Vivo, Staining, Immunohistochemical staining, Immunofluorescence, Comparison

    The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 8 weeks. HE staining (a), SO/FG staining (b), immunohistochemical staining of COLII (c) and MMP13 (d), immunofluorescence staining of CD86 (e) and CD206 (f) at the synovial, and immunofluorescence staining of IL-1β (g) in the TMJ of rats after 8 weeks of treatment, scale bar = 100 μm. (h) Histological OARSI score of articular cartilage after 8 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (b–g). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 8 weeks. HE staining (a), SO/FG staining (b), immunohistochemical staining of COLII (c) and MMP13 (d), immunofluorescence staining of CD86 (e) and CD206 (f) at the synovial, and immunofluorescence staining of IL-1β (g) in the TMJ of rats after 8 weeks of treatment, scale bar = 100 μm. (h) Histological OARSI score of articular cartilage after 8 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (b–g). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: In Vivo, Staining, Immunohistochemical staining, Immunofluorescence, Comparison

    The in vivo subchondral bone repair and regeneration effect of Mn-NC composite hydrogels on TMJ-OA after 2 and 8 weeks. (a, b) The temporomandibular joints of rats were collected at 2 and 8 weeks, three views of the condyles reconstructed by micro-CT scan (coronal, horizontal, and sagittal view), scale bar = 1 mm. Quantitative statistics of trabecular thickness (Tb. Th) (c), trabecular separation (Tb. Sp) (d), and ratios of bone volume (BV/TV) (e) from Sham, MIA, MIA + CH, MIA + CH@Mn2 at 2 and 8 weeks. (f) Trap staining images and quantification analysis after 2 weeks of hydrogels treatment. (g) Trap staining images and quantification analysis after 8 weeks of hydrogels treatment. (h) OPN staining images and quantification analysis after 8 weeks of hydrogels treatment. Data represent means ± SD, n = 3. ∗p < 0.05 and ∗∗p < 0.01 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: The in vivo subchondral bone repair and regeneration effect of Mn-NC composite hydrogels on TMJ-OA after 2 and 8 weeks. (a, b) The temporomandibular joints of rats were collected at 2 and 8 weeks, three views of the condyles reconstructed by micro-CT scan (coronal, horizontal, and sagittal view), scale bar = 1 mm. Quantitative statistics of trabecular thickness (Tb. Th) (c), trabecular separation (Tb. Sp) (d), and ratios of bone volume (BV/TV) (e) from Sham, MIA, MIA + CH, MIA + CH@Mn2 at 2 and 8 weeks. (f) Trap staining images and quantification analysis after 2 weeks of hydrogels treatment. (g) Trap staining images and quantification analysis after 8 weeks of hydrogels treatment. (h) OPN staining images and quantification analysis after 8 weeks of hydrogels treatment. Data represent means ± SD, n = 3. ∗p < 0.05 and ∗∗p < 0.01 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: In Vivo, Micro-CT, Staining, Comparison

    Underlying mechanism of Mn-NC SAzymes composite hydrogels in treating TMJ-OA. (a) The volcano plot showing the DEGs of IL-1β VS Control. (b) The volcano plot showing the DEGs of CH@Mn2 VS IL-1β. (c) Differential gene clustering thermogram of extracellular matrix organization (gray), regulation of inflammatory response (green) and cell adhesion molecule binding (purple) pathway. (d) Gene Ontology (GO) enrichment analysis of CH@Mn2 VS IL-1β. (e) The KEGG enrichment result of the DEGs of IL-1β VS Control. (f) The KEGG enrichment result of the DEGs of CH@Mn2 VS IL-1β. (g) Differential gene clustering thermogram of the MAPK pathway. (h) Activation of MAPK pathway after IL-1β stimulation. n = 3.

    Journal: Bioactive Materials

    Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

    doi: 10.1016/j.bioactmat.2026.01.031

    Figure Lengend Snippet: Underlying mechanism of Mn-NC SAzymes composite hydrogels in treating TMJ-OA. (a) The volcano plot showing the DEGs of IL-1β VS Control. (b) The volcano plot showing the DEGs of CH@Mn2 VS IL-1β. (c) Differential gene clustering thermogram of extracellular matrix organization (gray), regulation of inflammatory response (green) and cell adhesion molecule binding (purple) pathway. (d) Gene Ontology (GO) enrichment analysis of CH@Mn2 VS IL-1β. (e) The KEGG enrichment result of the DEGs of IL-1β VS Control. (f) The KEGG enrichment result of the DEGs of CH@Mn2 VS IL-1β. (g) Differential gene clustering thermogram of the MAPK pathway. (h) Activation of MAPK pathway after IL-1β stimulation. n = 3.

    Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

    Techniques: Control, Binding Assay, Activation Assay

    M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

    Journal: Bioactive Materials

    Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

    doi: 10.1016/j.bioactmat.2026.01.047

    Figure Lengend Snippet: M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

    Article Snippet: ELISA kits included mouse TNF- α ELISA kit (Solarbio), mouse IL-10 ELISA kit (Elabscience), mouse Hp ELISA kit (Elabscience), mouse IL-1β ELISA kit (Solarbio), and TGF-β ELISA kit (Solarbio).

    Techniques: In Vitro, Flow Cytometry, Fluorescence, Microscopy, Permeability, Transwell Assay

    iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

    Journal: Genes & Diseases

    Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

    doi: 10.1016/j.gendis.2025.101931

    Figure Lengend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

    Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

    Techniques: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

    Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.

    Journal: Genes & Diseases

    Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

    doi: 10.1016/j.gendis.2025.101931

    Figure Lengend Snippet: Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.

    Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

    Techniques: Recombinant, Activation Assay, Expressing, Western Blot, Two Tailed Test

    Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

    Journal: Genes & Diseases

    Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

    doi: 10.1016/j.gendis.2025.101931

    Figure Lengend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

    Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

    Techniques: Recombinant

    Prostaglandin dysregulation and inflammatory response in the RPP model (A–C) Uterine PGF 2α (A), PGE 2 (B), and PGF 2α /PGE 2 ratio (C) on days 12 and 24 of RPP modeling ( n = 3). (D) The protein levels of COX-2 in the uterine tissue on days 12 and 24 of RPP modeling ( n = 3). (E–G) The levels of IL-1β (E), IL-6 (F), and TNF-α (G) in the serum on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, one-way ANOVA.

    Journal: iScience

    Article Title: A pharmacological rat model of recurrent pelvic pain exhibiting hyperalgesia and depression-like behaviors

    doi: 10.1016/j.isci.2026.115059

    Figure Lengend Snippet: Prostaglandin dysregulation and inflammatory response in the RPP model (A–C) Uterine PGF 2α (A), PGE 2 (B), and PGF 2α /PGE 2 ratio (C) on days 12 and 24 of RPP modeling ( n = 3). (D) The protein levels of COX-2 in the uterine tissue on days 12 and 24 of RPP modeling ( n = 3). (E–G) The levels of IL-1β (E), IL-6 (F), and TNF-α (G) in the serum on days 12 and 24 of RPP modeling ( n = 3). Data are presented as the mean ± SD; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, one-way ANOVA.

    Article Snippet: Rat IL-1β ELISA Kit , Elabscience , Cat# E-EL-R0012.

    Techniques: