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Vazyme Biotech Co brightgreen apoptosis detection kit
Paeonol alleviates D-gal-induced <t>apoptosis</t> in GCs. A-E: qRT-PCR detection of BCL2 , Caspase-3, PCNA, CDK2 , and CCND1 . F-K: Western blot detection of Bax, Bcl-2, PCNA, Caspase-3, and CDK2 proteins. L-M: Annexin V/PI staining and flow cytometry analysis for detection of apoptosis; Q2: Annexin V⁺ / PI⁺, late apoptotic cells; Q3: Annexin V⁺ / PI⁻, early apoptotic cells. Data are presented as mean ± SEM ( n ≥ 3). Different lowercase letters indicate significant differences ( P < 0.05).
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Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of <t>apoptosis-related</t> proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) <t>Tunel</t> (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).
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Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of <t>apoptosis-related</t> proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) <t>Tunel</t> (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).
Tunel Assay Kit, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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COPN mitigates oxidative stress, neuroinflammation, and <t>apoptosis</t> in OHT-induced RIRI. a–f , Quantitative analyses of apoptotic markers (TuJ-1, Brn3A, Caspase-3, Bax, Cytochrome-c, and Bcl-2) in retinas subjected to various treatments, which revealed a significant reduction in COPN-induced apoptosis. g , <t>TUNEL</t> assay demonstrating reduced apoptosis in COPN-treated retinas (red fluorescence indicates apoptotic cells, and nuclei are stained with DAPI, blue). h–o , ELISA quantification of proinflammatory cytokines (TNF-α, IL-1β, IFN-γ, IL-18, and MCP-1) and oxidative stress markers (CAT, SOD, MDA, and MCP-1), demonstrating the broad anti-inflammatory and antioxidative effects of COPN. ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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The expression of interleukin-11 (IL-11) is increased in myocardial fibrosis in vitro and in vivo. A. Western blot analysis of IL-11 and vimentin expression in angiotensin II (AngII, 100 nM) or TGF-β (10 ng/mL)-treated cardiac fibroblasts. B. Quantification of (A). C. <t>TUNEL</t> staining and (D) its quantitative analysis in treated cells. E. CCK-8 viability assays (n = 3). F. Circulating IL-11 levels in mouse blood measured by ELISA (n = 3). ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.
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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 <t>apoptosis</t> 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.
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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 <t>apoptosis</t> 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.
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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 <t>apoptosis</t> 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.
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Image Search Results


Paeonol alleviates D-gal-induced apoptosis in GCs. A-E: qRT-PCR detection of BCL2 , Caspase-3, PCNA, CDK2 , and CCND1 . F-K: Western blot detection of Bax, Bcl-2, PCNA, Caspase-3, and CDK2 proteins. L-M: Annexin V/PI staining and flow cytometry analysis for detection of apoptosis; Q2: Annexin V⁺ / PI⁺, late apoptotic cells; Q3: Annexin V⁺ / PI⁻, early apoptotic cells. Data are presented as mean ± SEM ( n ≥ 3). Different lowercase letters indicate significant differences ( P < 0.05).

Journal: Poultry Science

Article Title: Paeonol alleviates granulosa cell senescence in laying chickens via the PI3K/Akt/mTOR signaling pathway

doi: 10.1016/j.psj.2026.106750

Figure Lengend Snippet: Paeonol alleviates D-gal-induced apoptosis in GCs. A-E: qRT-PCR detection of BCL2 , Caspase-3, PCNA, CDK2 , and CCND1 . F-K: Western blot detection of Bax, Bcl-2, PCNA, Caspase-3, and CDK2 proteins. L-M: Annexin V/PI staining and flow cytometry analysis for detection of apoptosis; Q2: Annexin V⁺ / PI⁺, late apoptotic cells; Q3: Annexin V⁺ / PI⁻, early apoptotic cells. Data are presented as mean ± SEM ( n ≥ 3). Different lowercase letters indicate significant differences ( P < 0.05).

Article Snippet: Deparaffinized sections were processed using a BrightGreen Apoptosis Detection Kit (A112-03, Vazyme, Nanjing, China) according to the manufacturer's protocol.

Techniques: Quantitative RT-PCR, Western Blot, Staining, Flow Cytometry

Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Journal: Bioactive Materials

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Article Snippet: Additionally, apoptosis was independently assessed by using a One-step TUNEL In Situ Apoptosis Kit (E-CK-A322, Elabscience, Wuhan, China) according to the manufacturer's instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Staining, Flow Cytometry, TUNEL Assay, In Vitro

The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Journal: Bioactive Materials

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Article Snippet: Additionally, apoptosis was independently assessed by using a One-step TUNEL In Situ Apoptosis Kit (E-CK-A322, Elabscience, Wuhan, China) according to the manufacturer's instructions.

Techniques: MTT Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Flow Cytometry, TUNEL Assay, In Vitro

Summary of the study. The schematic diagram illustrates that DUB alleviates GIOP by suppressing oxidative stress and apoptosis via the CD39/CD73/ADO axis and promotes osteogenesis via ADO/A 2b R-mediated activation of the PKA/CREB pathway. The schematic diagram was created by using BioRender.com.

Journal: Bioactive Materials

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Summary of the study. The schematic diagram illustrates that DUB alleviates GIOP by suppressing oxidative stress and apoptosis via the CD39/CD73/ADO axis and promotes osteogenesis via ADO/A 2b R-mediated activation of the PKA/CREB pathway. The schematic diagram was created by using BioRender.com.

Article Snippet: Additionally, apoptosis was independently assessed by using a One-step TUNEL In Situ Apoptosis Kit (E-CK-A322, Elabscience, Wuhan, China) according to the manufacturer's instructions.

Techniques: Activation Assay

COPN mitigates oxidative stress, neuroinflammation, and apoptosis in OHT-induced RIRI. a–f , Quantitative analyses of apoptotic markers (TuJ-1, Brn3A, Caspase-3, Bax, Cytochrome-c, and Bcl-2) in retinas subjected to various treatments, which revealed a significant reduction in COPN-induced apoptosis. g , TUNEL assay demonstrating reduced apoptosis in COPN-treated retinas (red fluorescence indicates apoptotic cells, and nuclei are stained with DAPI, blue). h–o , ELISA quantification of proinflammatory cytokines (TNF-α, IL-1β, IFN-γ, IL-18, and MCP-1) and oxidative stress markers (CAT, SOD, MDA, and MCP-1), demonstrating the broad anti-inflammatory and antioxidative effects of COPN. ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Journal: Materials Today Bio

Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

doi: 10.1016/j.mtbio.2026.102974

Figure Lengend Snippet: COPN mitigates oxidative stress, neuroinflammation, and apoptosis in OHT-induced RIRI. a–f , Quantitative analyses of apoptotic markers (TuJ-1, Brn3A, Caspase-3, Bax, Cytochrome-c, and Bcl-2) in retinas subjected to various treatments, which revealed a significant reduction in COPN-induced apoptosis. g , TUNEL assay demonstrating reduced apoptosis in COPN-treated retinas (red fluorescence indicates apoptotic cells, and nuclei are stained with DAPI, blue). h–o , ELISA quantification of proinflammatory cytokines (TNF-α, IL-1β, IFN-γ, IL-18, and MCP-1) and oxidative stress markers (CAT, SOD, MDA, and MCP-1), demonstrating the broad anti-inflammatory and antioxidative effects of COPN. ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was performed via the TUNEL BrightRed Apoptosis Detection Kit (Vazyme, Cat# A113-01) according to the manufacturer's instructions.

Techniques: TUNEL Assay, Fluorescence, Staining, Enzyme-linked Immunosorbent Assay

COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Journal: Materials Today Bio

Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

doi: 10.1016/j.mtbio.2026.102974

Figure Lengend Snippet: COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was performed via the TUNEL BrightRed Apoptosis Detection Kit (Vazyme, Cat# A113-01) according to the manufacturer's instructions.

Techniques: Quantitative Proteomics, Control, Activation Assay, Phospho-proteomics, Disruption, Western Blot

The expression of interleukin-11 (IL-11) is increased in myocardial fibrosis in vitro and in vivo. A. Western blot analysis of IL-11 and vimentin expression in angiotensin II (AngII, 100 nM) or TGF-β (10 ng/mL)-treated cardiac fibroblasts. B. Quantification of (A). C. TUNEL staining and (D) its quantitative analysis in treated cells. E. CCK-8 viability assays (n = 3). F. Circulating IL-11 levels in mouse blood measured by ELISA (n = 3). ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Journal: Bioactive Materials

Article Title: Ameliorating post-infarction myocardial fibrosis and cardiac function via ROS-responsive hydrogel-mediated IL-11 antibody delivery

doi: 10.1016/j.bioactmat.2026.01.041

Figure Lengend Snippet: The expression of interleukin-11 (IL-11) is increased in myocardial fibrosis in vitro and in vivo. A. Western blot analysis of IL-11 and vimentin expression in angiotensin II (AngII, 100 nM) or TGF-β (10 ng/mL)-treated cardiac fibroblasts. B. Quantification of (A). C. TUNEL staining and (D) its quantitative analysis in treated cells. E. CCK-8 viability assays (n = 3). F. Circulating IL-11 levels in mouse blood measured by ELISA (n = 3). ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Sections were fixed in 4 % PFA for 30 min, permeabilized, and blocked with DAKO solution (0.1 % saponin) for 1 h. Apoptosis was detected using the One Step TUNEL Apoptosis Kit (Beyotime, C1089) per manufacturer's instructions.

Techniques: Expressing, In Vitro, In Vivo, Western Blot, TUNEL Assay, Staining, CCK-8 Assay, Enzyme-linked Immunosorbent Assay

P-T@MAB injection promotes angiomyogenesis. Immunostaining images show TUNEL at 3 days post-injection (A), Ki67 (C), vWF (E), and CD31 (F) expression in heart sections at 4 weeks post-injection. Quantitative analysis of TUNEL (B), Ki67 (D), vWF (G), and CD31 (G) is presented (n = 5). Scale bars: 100 μm. n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Journal: Bioactive Materials

Article Title: Ameliorating post-infarction myocardial fibrosis and cardiac function via ROS-responsive hydrogel-mediated IL-11 antibody delivery

doi: 10.1016/j.bioactmat.2026.01.041

Figure Lengend Snippet: P-T@MAB injection promotes angiomyogenesis. Immunostaining images show TUNEL at 3 days post-injection (A), Ki67 (C), vWF (E), and CD31 (F) expression in heart sections at 4 weeks post-injection. Quantitative analysis of TUNEL (B), Ki67 (D), vWF (G), and CD31 (G) is presented (n = 5). Scale bars: 100 μm. n.s., not significant; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Sections were fixed in 4 % PFA for 30 min, permeabilized, and blocked with DAKO solution (0.1 % saponin) for 1 h. Apoptosis was detected using the One Step TUNEL Apoptosis Kit (Beyotime, C1089) per manufacturer's instructions.

Techniques: Injection, Immunostaining, TUNEL Assay, Expressing

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: TUNEL staining was performed using a TUNEL Apoptosis Assay Kit (red fluorescence; Beyotime Biotechnology Company, China).

Techniques: Activity Assay

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: TUNEL staining was performed using a TUNEL Apoptosis Assay Kit (red fluorescence; Beyotime Biotechnology Company, China).

Techniques: Staining, Flow Cytometry, Control, Comparison

Schematic diagram illustrates the mechanism of Mn-NC SAzymes composite hydrogel inhibiting excessive activation of the MAPK signaling pathway, thereby suppressing inflammatory responses, extracellular matrix degradation, and cell apoptosis during the pathogenesis of TMJ-OA.

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 SAzymes composite hydrogel inhibiting excessive activation of the MAPK signaling pathway, thereby suppressing inflammatory responses, extracellular matrix degradation, and cell apoptosis during the pathogenesis of TMJ-OA.

Article Snippet: TUNEL staining was performed using a TUNEL Apoptosis Assay Kit (red fluorescence; Beyotime Biotechnology Company, China).

Techniques: Activation Assay