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Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of <t>COL2A1,</t> SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).
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Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of <t>COL2A1,</t> SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).
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Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of <t>COL2A1,</t> SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).
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Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of <t>COL2A1,</t> SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).
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DS@CAD ameliorates TNF-α-induced imbalance between anabolism and catabolism in HNPCs. (A) Heatmap visualization of RT‒qPCR data showing the expression of ECM synthesis markers <t>(Col2a1,</t> COL1 and Acan), degradation markers (Adamts4 and MMP13), and inflammation indicators (COX2 and iNOS) after different treatments. (B) Western blot analysis was used to evaluate ECM synthesis proteins (Col2a1, COL1 and Acan), degradation proteins (Adamts4 and MMP13), and inflammation markers (COX2 and iNOS) following different interventions. (C–H) Quantitative analysis of the Western blot data. (I, J) Alcian blue and Safranin O staining of NPCs after various treatments (scale bar: 200 μm). (K) IF of Col2a1, MMP13, and COX2 in NPCs after different treatments (scale bar: 20 μm). (L, M). Relative statistics of Alcian and Safranin O staining. (N–P) Statistical analysis of fluorescence intensity in the IF analysis. (n = 3; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).
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Post-operative histological analysis of osteochondral defect sections after 12 weeks. (a) Hematoxylin and eosin (H&E), Safranin O, Masson's trichrome (MT), and collagen II immunohistological staining. Scale bar = 200 μm. Black arrowheads indicate the defect margins. Dashed lines indicate the regenerated areas. (b) Quantification of <t>Safranin</t> <t>O</t> and collagen II expression based on the immunohistological staining results. (c) Modified O'Driscoll histological total score. Scoring criteria is provided in the Supplementary Information . ## indicates significant difference compared to the defect group with p < 0.05 and ∗ and ∗∗ indicate significant differences between the indicated groups with p < 0.05 and p < 0.01, respectively (n = 6).
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Image Search Results


Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of COL2A1, SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of COL2A1, SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: Immunofluorescence, Expressing

Expression analysis of cartilage-related proteins after treatment with AdHy@Pae. (A) Representative Western blot images showing ECM synthesis–related proteins (COL2A1, ACAN, COMP, and SOX9) and antioxidant markers (NRF2 and HO-1) in different groups. (B) Quantitative analysis of matrix-degrading enzymes (MMP13, ADAMTS5, ADAMTS1) and apoptosis-related proteins (BCL-2, Bax, and Caspase-3). Data are presented as mean ± SD (n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: Expression analysis of cartilage-related proteins after treatment with AdHy@Pae. (A) Representative Western blot images showing ECM synthesis–related proteins (COL2A1, ACAN, COMP, and SOX9) and antioxidant markers (NRF2 and HO-1) in different groups. (B) Quantitative analysis of matrix-degrading enzymes (MMP13, ADAMTS5, ADAMTS1) and apoptosis-related proteins (BCL-2, Bax, and Caspase-3). Data are presented as mean ± SD (n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: Expressing, Western Blot

In vivo validation of the chondroprotective and mitochondrial regulatory effects of AdHy@Pae after therapy for 4 weeks. (A) Representative immunohistochemical staining of cartilage sections for COL2A1, SOX9, MMP3, and ADAMTS1 in different groups (Sham, PBS, Hy, AdHy, and AdHy@Pae). (B) Quantitative analysis of the immunohistochemical staining intensity showing relative expression levels of anabolic (COL2A1, SOX9) and catabolic (MMP3, ADAMTS1) markers. (C) TEM images of chondrocytes showing mitochondrial ultrastructure in each group, with high-magnification views (bottom panels) indicating cristae integrity and membrane morphology. Data are presented as mean ± SD (n = 3); ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗P < 0.0001.

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: In vivo validation of the chondroprotective and mitochondrial regulatory effects of AdHy@Pae after therapy for 4 weeks. (A) Representative immunohistochemical staining of cartilage sections for COL2A1, SOX9, MMP3, and ADAMTS1 in different groups (Sham, PBS, Hy, AdHy, and AdHy@Pae). (B) Quantitative analysis of the immunohistochemical staining intensity showing relative expression levels of anabolic (COL2A1, SOX9) and catabolic (MMP3, ADAMTS1) markers. (C) TEM images of chondrocytes showing mitochondrial ultrastructure in each group, with high-magnification views (bottom panels) indicating cristae integrity and membrane morphology. Data are presented as mean ± SD (n = 3); ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗P < 0.0001.

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: In Vivo, Biomarker Discovery, Immunohistochemical staining, Staining, Expressing, Membrane

DS@CAD ameliorates TNF-α-induced imbalance between anabolism and catabolism in HNPCs. (A) Heatmap visualization of RT‒qPCR data showing the expression of ECM synthesis markers (Col2a1, COL1 and Acan), degradation markers (Adamts4 and MMP13), and inflammation indicators (COX2 and iNOS) after different treatments. (B) Western blot analysis was used to evaluate ECM synthesis proteins (Col2a1, COL1 and Acan), degradation proteins (Adamts4 and MMP13), and inflammation markers (COX2 and iNOS) following different interventions. (C–H) Quantitative analysis of the Western blot data. (I, J) Alcian blue and Safranin O staining of NPCs after various treatments (scale bar: 200 μm). (K) IF of Col2a1, MMP13, and COX2 in NPCs after different treatments (scale bar: 20 μm). (L, M). Relative statistics of Alcian and Safranin O staining. (N–P) Statistical analysis of fluorescence intensity in the IF analysis. (n = 3; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Journal: Materials Today Bio

Article Title: Sequential delivery of sinigrin and dabigatran by an in situ self-stabilizing dynamic hydrogel attenuates intervertebral disc degeneration

doi: 10.1016/j.mtbio.2026.102827

Figure Lengend Snippet: DS@CAD ameliorates TNF-α-induced imbalance between anabolism and catabolism in HNPCs. (A) Heatmap visualization of RT‒qPCR data showing the expression of ECM synthesis markers (Col2a1, COL1 and Acan), degradation markers (Adamts4 and MMP13), and inflammation indicators (COX2 and iNOS) after different treatments. (B) Western blot analysis was used to evaluate ECM synthesis proteins (Col2a1, COL1 and Acan), degradation proteins (Adamts4 and MMP13), and inflammation markers (COX2 and iNOS) following different interventions. (C–H) Quantitative analysis of the Western blot data. (I, J) Alcian blue and Safranin O staining of NPCs after various treatments (scale bar: 200 μm). (K) IF of Col2a1, MMP13, and COX2 in NPCs after different treatments (scale bar: 20 μm). (L, M). Relative statistics of Alcian and Safranin O staining. (N–P) Statistical analysis of fluorescence intensity in the IF analysis. (n = 3; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Article Snippet: Cells in glass-bottomed dishes were sequentially treated: fixed with 4 % paraformaldehyde for 20 min, permeabilized with 0.5 % Triton X-100 for 15 min, and blocked with 5 % (w/v) bovine serum albumin for 30 min, before incubation with primary antibodies against Col2a1 (1:100, A19308, abclone, China), MMP13 (A1606, abclone, China), COX2 (27308-1-AP, Proteintech, China).

Techniques: Expressing, Western Blot, Staining, Fluorescence

DS@CAD directly promotes the anabolic activity of NPCs. (A): RT‒PCR results showing the expression of ECM synthesis markers (Acan, Col2a1, and SOX9). (B) ELISA analysis of COMP concentration. (C, D) Safranin O and Alcian blue staining of NPCs after various treatments. (E) Western blot results for ECM synthesis proteins. (F, G) IF of Acan and Col2a1 in NPCs after different treatments. (H, I) Statistical analysis of the Alcian and Safranin O staining results. (J) Quantitative analysis of the Western blot data. (K) Statistical analysis of the fluorescence intensity in the IF analysis. (n = 3; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Journal: Materials Today Bio

Article Title: Sequential delivery of sinigrin and dabigatran by an in situ self-stabilizing dynamic hydrogel attenuates intervertebral disc degeneration

doi: 10.1016/j.mtbio.2026.102827

Figure Lengend Snippet: DS@CAD directly promotes the anabolic activity of NPCs. (A): RT‒PCR results showing the expression of ECM synthesis markers (Acan, Col2a1, and SOX9). (B) ELISA analysis of COMP concentration. (C, D) Safranin O and Alcian blue staining of NPCs after various treatments. (E) Western blot results for ECM synthesis proteins. (F, G) IF of Acan and Col2a1 in NPCs after different treatments. (H, I) Statistical analysis of the Alcian and Safranin O staining results. (J) Quantitative analysis of the Western blot data. (K) Statistical analysis of the fluorescence intensity in the IF analysis. (n = 3; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Article Snippet: Cells in glass-bottomed dishes were sequentially treated: fixed with 4 % paraformaldehyde for 20 min, permeabilized with 0.5 % Triton X-100 for 15 min, and blocked with 5 % (w/v) bovine serum albumin for 30 min, before incubation with primary antibodies against Col2a1 (1:100, A19308, abclone, China), MMP13 (A1606, abclone, China), COX2 (27308-1-AP, Proteintech, China).

Techniques: Activity Assay, Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Staining, Western Blot, Fluorescence

DS@CAD protects against IDD in a surgically induced model in vivo. (A) Procedural flow for in vivo experiments in rats (created using BioRender.com ). (B) Micro-CT and (C) MR images of the punctured disc segments at 4 weeks and 8 weeks posttreatment. (D) Representative images of H&E staining in each group at 4 and 8 weeks. (E) Representative images of SO&FG staining in each group at 4 and 8 weeks. (F) IHC staining image of Col2a1, MMP13 and COX2 at 8 weeks. (G, H) Differences in the DHI between each group at 4 and 8 weeks. (I) Quantitative analysis of the average grey value of IVDs. (J) Heatmap showing Pfirrmann grade differences within each group at 4 and 8 weeks. (K) Histological grades of the different groups at weeks 4 and 8. (n = 5; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Journal: Materials Today Bio

Article Title: Sequential delivery of sinigrin and dabigatran by an in situ self-stabilizing dynamic hydrogel attenuates intervertebral disc degeneration

doi: 10.1016/j.mtbio.2026.102827

Figure Lengend Snippet: DS@CAD protects against IDD in a surgically induced model in vivo. (A) Procedural flow for in vivo experiments in rats (created using BioRender.com ). (B) Micro-CT and (C) MR images of the punctured disc segments at 4 weeks and 8 weeks posttreatment. (D) Representative images of H&E staining in each group at 4 and 8 weeks. (E) Representative images of SO&FG staining in each group at 4 and 8 weeks. (F) IHC staining image of Col2a1, MMP13 and COX2 at 8 weeks. (G, H) Differences in the DHI between each group at 4 and 8 weeks. (I) Quantitative analysis of the average grey value of IVDs. (J) Heatmap showing Pfirrmann grade differences within each group at 4 and 8 weeks. (K) Histological grades of the different groups at weeks 4 and 8. (n = 5; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001).

Article Snippet: Cells in glass-bottomed dishes were sequentially treated: fixed with 4 % paraformaldehyde for 20 min, permeabilized with 0.5 % Triton X-100 for 15 min, and blocked with 5 % (w/v) bovine serum albumin for 30 min, before incubation with primary antibodies against Col2a1 (1:100, A19308, abclone, China), MMP13 (A1606, abclone, China), COX2 (27308-1-AP, Proteintech, China).

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

Molecular mechanism of DAB in ECM synthesis. (A) Volcano plot shows the DEG significance and fold change (CTR vs. DAB). (B) KEGG enrichment of the DEG pathways (CTR vs. DAB). (C) GSEA identified AMPK pathway enrichment. (D) Effects of DAB treatment duration (0, 10, 15, 30, 60, and 90 min) on protein levels in NPCs. (E) NPCs were treated with different concentrations of DAB (0, 0.5, 1.0, 5.0, and 10 μM). (F) Quantification of p-AMPK/AMPK protein levels. (G) P-AMPK and AMPK expression after 15 and 30 min of DAB ± Compound C treatment. (H) P-AMPK and AMPK expression following DAB treatment (1 and 10 μM) ± Compound C. (I) Quantification of p-AMPK/AMPK protein levels. (J–L) Col2a1 and Acan protein levels and IF results after DAB (5 and 10 μM) ± Compound C treatment. (M, N) Quantification and immunofluorescence analysis of Acan and Col2a1 protein expression. (n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001).

Journal: Materials Today Bio

Article Title: Sequential delivery of sinigrin and dabigatran by an in situ self-stabilizing dynamic hydrogel attenuates intervertebral disc degeneration

doi: 10.1016/j.mtbio.2026.102827

Figure Lengend Snippet: Molecular mechanism of DAB in ECM synthesis. (A) Volcano plot shows the DEG significance and fold change (CTR vs. DAB). (B) KEGG enrichment of the DEG pathways (CTR vs. DAB). (C) GSEA identified AMPK pathway enrichment. (D) Effects of DAB treatment duration (0, 10, 15, 30, 60, and 90 min) on protein levels in NPCs. (E) NPCs were treated with different concentrations of DAB (0, 0.5, 1.0, 5.0, and 10 μM). (F) Quantification of p-AMPK/AMPK protein levels. (G) P-AMPK and AMPK expression after 15 and 30 min of DAB ± Compound C treatment. (H) P-AMPK and AMPK expression following DAB treatment (1 and 10 μM) ± Compound C. (I) Quantification of p-AMPK/AMPK protein levels. (J–L) Col2a1 and Acan protein levels and IF results after DAB (5 and 10 μM) ± Compound C treatment. (M, N) Quantification and immunofluorescence analysis of Acan and Col2a1 protein expression. (n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001).

Article Snippet: Cells in glass-bottomed dishes were sequentially treated: fixed with 4 % paraformaldehyde for 20 min, permeabilized with 0.5 % Triton X-100 for 15 min, and blocked with 5 % (w/v) bovine serum albumin for 30 min, before incubation with primary antibodies against Col2a1 (1:100, A19308, abclone, China), MMP13 (A1606, abclone, China), COX2 (27308-1-AP, Proteintech, China).

Techniques: Expressing, Immunofluorescence

Post-operative histological analysis of osteochondral defect sections after 12 weeks. (a) Hematoxylin and eosin (H&E), Safranin O, Masson's trichrome (MT), and collagen II immunohistological staining. Scale bar = 200 μm. Black arrowheads indicate the defect margins. Dashed lines indicate the regenerated areas. (b) Quantification of Safranin O and collagen II expression based on the immunohistological staining results. (c) Modified O'Driscoll histological total score. Scoring criteria is provided in the Supplementary Information . ## indicates significant difference compared to the defect group with p < 0.05 and ∗ and ∗∗ indicate significant differences between the indicated groups with p < 0.05 and p < 0.01, respectively (n = 6).

Journal: Materials Today Bio

Article Title: Hyaluronan open-pit nanofibrils with spontaneous cell-matrix assembly for advanced osteochondral defect repair

doi: 10.1016/j.mtbio.2026.102986

Figure Lengend Snippet: Post-operative histological analysis of osteochondral defect sections after 12 weeks. (a) Hematoxylin and eosin (H&E), Safranin O, Masson's trichrome (MT), and collagen II immunohistological staining. Scale bar = 200 μm. Black arrowheads indicate the defect margins. Dashed lines indicate the regenerated areas. (b) Quantification of Safranin O and collagen II expression based on the immunohistological staining results. (c) Modified O'Driscoll histological total score. Scoring criteria is provided in the Supplementary Information . ## indicates significant difference compared to the defect group with p < 0.05 and ∗ and ∗∗ indicate significant differences between the indicated groups with p < 0.05 and p < 0.01, respectively (n = 6).

Article Snippet: Transverse sections of 5 μm-thickness from the central area of the defect site were produced using a microtome, which were subsequently de-paraffinized and re-hydrated before staining with hematoxylin and eosin (H&E), Safranin O, Masson's trichrome (MT), and antibodies against collagen type II (SC-517571; Santa Cruz Biotechnology, CA).

Techniques: Staining, Expressing, Modification