Review



antibodies targeting col2a1  (Proteintech)


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    Structured Review

    Proteintech antibodies targeting col2a1
    qPCR primer information.
    Antibodies Targeting Col2a1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 606 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/col2a1/Collagen+Type+II+Antibody/pmc13658529-179-7-10
    Average 96 stars, based on 606 article reviews
    antibodies targeting col2a1 - by Bioz Stars, 2026-10
    96/100 stars

    Images

    1) Product Images from "pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis"

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    Journal: Frontiers in Bioengineering and Biotechnology

    doi: 10.3389/fbioe.2026.1924086

    qPCR primer information.
    Figure Legend Snippet: qPCR primer information.

    Techniques Used: Sequencing

    PGG-Zn@Cur restored matrix metabolic homeostasis in IL-1β-stimulated chondrocytes. (A) Representative immunofluorescence images of COL2A1 in chondrocytes after different treatments. COL2A1 was stained red, and nuclei were counterstained with DAPI. (B) Representative immunofluorescence images of MMP13 in chondrocytes after different treatments. MMP13 was stained green, and nuclei were counterstained with DAPI. (C) Quantitative analysis of relative fluorescence intensity for COL2A1 and MMP13 based on immunofluorescence staining. IL-1β stimulation decreased COL2A1 expression and increased MMP13 accumulation, whereas PGG-Zn@Cur treatment restored COL2A1 fluorescence intensity and suppressed MMP13-positive signals. (D–G) RT-qPCR analysis of cartilage matrix metabolism-related genes, including anabolic markers Col2a1 and Aggrecan, and catabolic markers Mmp13 and Adamts5, in chondrocytes after the indicated treatments. (H) Representative Western blot images of iNOS, COL2A1, MMP13, and ACAN protein expression, together with heatmap-based quantitative analysis of Western blot results across different treatment groups. β-Actin was used as the loading control. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: no significant).
    Figure Legend Snippet: PGG-Zn@Cur restored matrix metabolic homeostasis in IL-1β-stimulated chondrocytes. (A) Representative immunofluorescence images of COL2A1 in chondrocytes after different treatments. COL2A1 was stained red, and nuclei were counterstained with DAPI. (B) Representative immunofluorescence images of MMP13 in chondrocytes after different treatments. MMP13 was stained green, and nuclei were counterstained with DAPI. (C) Quantitative analysis of relative fluorescence intensity for COL2A1 and MMP13 based on immunofluorescence staining. IL-1β stimulation decreased COL2A1 expression and increased MMP13 accumulation, whereas PGG-Zn@Cur treatment restored COL2A1 fluorescence intensity and suppressed MMP13-positive signals. (D–G) RT-qPCR analysis of cartilage matrix metabolism-related genes, including anabolic markers Col2a1 and Aggrecan, and catabolic markers Mmp13 and Adamts5, in chondrocytes after the indicated treatments. (H) Representative Western blot images of iNOS, COL2A1, MMP13, and ACAN protein expression, together with heatmap-based quantitative analysis of Western blot results across different treatment groups. β-Actin was used as the loading control. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: no significant).

    Techniques Used: Immunofluorescence, Staining, Analysis, Fluorescence, Expressing, Quantitative RT-PCR, Western Blot, Control

    PGG-Zn@Cur attenuated PI3K-AKT activation and apoptosis-associated responses in IL-1β-stimulated chondrocytes. (A) Schematic workflow of RNA sequencing and subsequent experimental validation. (B) Heatmap of representative differentially expressed genes related to cartilage matrix metabolism, inflammation, apoptosis, and PI3K-AKT-associated signaling. (C) Volcano plot showing differentially expressed genes between the indicated groups, with representative genes related to cartilage homeostasis, apoptosis, and PI3K-AKT signaling labeled. (D) GO enrichment analysis of differentially expressed genes, including biological process, cellular component, and molecular function categories. (E) KEGG pathway enrichment analysis, with the PI3K-AKT signaling pathway highlighted as a candidate pathway. (F) Representative immunofluorescence images of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 in chondrocytes after different treatments. Nuclei were counterstained with DAPI. (G) Quantitative analysis of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 fluorescence intensity. (H) Representative Western blot images of PI3K-AKT pathway- and apoptosis-related proteins, including p-PI3K, PI3K, p-AKT, AKT, Cleaved-Caspase3, Caspase3, Bax, and BCL2. β-Actin was used as the loading control. (I) Heatmap-based quantitative analysis of Western blot results, summarizing changes in p-PI3K/PI3K, p-AKT/AKT, Cleaved-Caspase3/Caspase3, Bax/β-Actin, and BCL2/β-Actin across different groups. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).
    Figure Legend Snippet: PGG-Zn@Cur attenuated PI3K-AKT activation and apoptosis-associated responses in IL-1β-stimulated chondrocytes. (A) Schematic workflow of RNA sequencing and subsequent experimental validation. (B) Heatmap of representative differentially expressed genes related to cartilage matrix metabolism, inflammation, apoptosis, and PI3K-AKT-associated signaling. (C) Volcano plot showing differentially expressed genes between the indicated groups, with representative genes related to cartilage homeostasis, apoptosis, and PI3K-AKT signaling labeled. (D) GO enrichment analysis of differentially expressed genes, including biological process, cellular component, and molecular function categories. (E) KEGG pathway enrichment analysis, with the PI3K-AKT signaling pathway highlighted as a candidate pathway. (F) Representative immunofluorescence images of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 in chondrocytes after different treatments. Nuclei were counterstained with DAPI. (G) Quantitative analysis of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 fluorescence intensity. (H) Representative Western blot images of PI3K-AKT pathway- and apoptosis-related proteins, including p-PI3K, PI3K, p-AKT, AKT, Cleaved-Caspase3, Caspase3, Bax, and BCL2. β-Actin was used as the loading control. (I) Heatmap-based quantitative analysis of Western blot results, summarizing changes in p-PI3K/PI3K, p-AKT/AKT, Cleaved-Caspase3/Caspase3, Bax/β-Actin, and BCL2/β-Actin across different groups. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Techniques Used: Activation Assay, RNA Sequencing, Biomarker Discovery, Labeling, Analysis, Immunofluorescence, Fluorescence, Western Blot, Control

    PGG-Zn@Cur attenuates OA-associated cartilage degeneration and preserves matrix homeostasis in vivo . (A) Representative Safranin O/Fast Green staining images of knee joint cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. (B) Representative immunofluorescence images of COL2A1 and MMP13 in articular cartilage from different groups. Nuclei were counterstained with DAPI. (C, D) Quantitative analysis of cartilage degeneration using OARSI scores and modified Mankin’s scores. (E) Quantitative analysis of COL2A1 and MMP13 fluorescence intensity in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).
    Figure Legend Snippet: PGG-Zn@Cur attenuates OA-associated cartilage degeneration and preserves matrix homeostasis in vivo . (A) Representative Safranin O/Fast Green staining images of knee joint cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. (B) Representative immunofluorescence images of COL2A1 and MMP13 in articular cartilage from different groups. Nuclei were counterstained with DAPI. (C, D) Quantitative analysis of cartilage degeneration using OARSI scores and modified Mankin’s scores. (E) Quantitative analysis of COL2A1 and MMP13 fluorescence intensity in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Techniques Used: In Vivo, Staining, Immunofluorescence, Analysis, Modification, Fluorescence

    PGG-Zn@Cur attenuates PI3K-AKT pathway activation and apoptosis-associated cartilage damage in vivo . (A) Representative immunofluorescence images of p-PI3K, p-AKT, and COL2A1 in articular cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. Nuclei were counterstained with DAPI. (B) Representative TUNEL staining images of articular cartilage from different groups. (C) Quantitative analysis of p-PI3K, p-AKT, and COL2A1 fluorescence intensity in articular cartilage. (D) Quantitative analysis of TUNEL-positive chondrocytes in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).
    Figure Legend Snippet: PGG-Zn@Cur attenuates PI3K-AKT pathway activation and apoptosis-associated cartilage damage in vivo . (A) Representative immunofluorescence images of p-PI3K, p-AKT, and COL2A1 in articular cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. Nuclei were counterstained with DAPI. (B) Representative TUNEL staining images of articular cartilage from different groups. (C) Quantitative analysis of p-PI3K, p-AKT, and COL2A1 fluorescence intensity in articular cartilage. (D) Quantitative analysis of TUNEL-positive chondrocytes in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Techniques Used: Activation Assay, In Vivo, Immunofluorescence, TUNEL Assay, Staining, Analysis, Fluorescence

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    Western Blot:

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    Immunofluorescence:

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    Flow Cytometry:

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    Incubation:

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    Article Title: KLK8 promotes cartilage degradation and pyroptosis in osteoarthritis by activating the NF-κB and NLRP3 inflammasome pathways.
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    other:

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    Article Snippet: Following three gentle PBS washes, intracellular ROS was acquired on a BD LSRFortessa X-20 flow cytometer (excitation 488 nm, emission 525 nm) and quantified in FlowJo to assess oxidative stress across groups.

    Cytometry:

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    Tissue:

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    Electrophoresis:

    Article Title: KLK8 promotes cartilage degradation and pyroptosis in osteoarthritis by activating the NF-κB and NLRP3 inflammasome pathways.
    Article Snippet: Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment.. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA.. KLK8 expression was detected in meniscal/ligamentous injury (MLI)induced OA mouse models and human OA cartilage tissues.

    Membrane:

    Article Title: KLK8 promotes cartilage degradation and pyroptosis in osteoarthritis by activating the NF-κB and NLRP3 inflammasome pathways.
    Article Snippet: Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment.. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA.. KLK8 expression was detected in meniscal/ligamentous injury (MLI)induced OA mouse models and human OA cartilage tissues.

    Binding Assay:

    Article Title: KLK8 promotes cartilage degradation and pyroptosis in osteoarthritis by activating the NF-κB and NLRP3 inflammasome pathways.
    Article Snippet: Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment.. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA.. KLK8 expression was detected in meniscal/ligamentous injury (MLI)induced OA mouse models and human OA cartilage tissues.

    Blocking Assay:

    Article Title: KLK8 promotes cartilage degradation and pyroptosis in osteoarthritis by activating the NF-κB and NLRP3 inflammasome pathways.
    Article Snippet: Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment.. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA.. KLK8 expression was detected in meniscal/ligamentous injury (MLI)induced OA mouse models and human OA cartilage tissues.

    Article Title: An intelligent nanoliposome alleviates disc degeneration and discogenic pain by inhibiting neurovascular ingrowth via a “Soil-conditioning, seed-modulating, and weeds-suppressing” strategy
    Article Snippet: .. For immunofluorescence (IF) staining, antigen retrieval was conducted using citrate buffer (0.1 M, pH 6.0), followed by blocking in 10 % normal goat serum (Solarbio, Cat. No. SL038) at room temperature for 1 h. Sections were incubated overnight at 4 °C with primary antibodies targeting ACAN (Cat. No. DF7561, Affinity), COL2A1 (Cat. No. AF0135, Affinity), MMP3 (Cat. No. AF0217, Affinity), MMP13 (Cat. No. 18165-1-AP, Proteintech), CD31 (Cat. No. AF0077, Affinity), p-LATS1 (Cat. No. AF7170, Affinity), p-YAP (Cat. No. AF3328, Affinity), Tuj1 (Cat. No. 66375, Proteintech), CGRP (Cat. No. DF7386, Affinity), SP (Cat. No. DF7522, Affinity), and PGP9.5 (Cat. No. AF5490, Affinity) followed by incubation with appropriate fluorescent secondary antibodies for 2 h at room temperature and counterstaining with DAPI (Beyotime, Cat. No. C1006). .. Fluorescence images were acquired using a BX53 microscope (Olympus), and signal intensity was quantified with ImageJ software.

    Staining:

    Article Title: An intelligent nanoliposome alleviates disc degeneration and discogenic pain by inhibiting neurovascular ingrowth via a “Soil-conditioning, seed-modulating, and weeds-suppressing” strategy
    Article Snippet: .. For immunofluorescence (IF) staining, antigen retrieval was conducted using citrate buffer (0.1 M, pH 6.0), followed by blocking in 10 % normal goat serum (Solarbio, Cat. No. SL038) at room temperature for 1 h. Sections were incubated overnight at 4 °C with primary antibodies targeting ACAN (Cat. No. DF7561, Affinity), COL2A1 (Cat. No. AF0135, Affinity), MMP3 (Cat. No. AF0217, Affinity), MMP13 (Cat. No. 18165-1-AP, Proteintech), CD31 (Cat. No. AF0077, Affinity), p-LATS1 (Cat. No. AF7170, Affinity), p-YAP (Cat. No. AF3328, Affinity), Tuj1 (Cat. No. 66375, Proteintech), CGRP (Cat. No. DF7386, Affinity), SP (Cat. No. DF7522, Affinity), and PGP9.5 (Cat. No. AF5490, Affinity) followed by incubation with appropriate fluorescent secondary antibodies for 2 h at room temperature and counterstaining with DAPI (Beyotime, Cat. No. C1006). .. Fluorescence images were acquired using a BX53 microscope (Olympus), and signal intensity was quantified with ImageJ software.

    Cell Culture:

    Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration
    Article Snippet: Following three gentle PBS washes, intracellular ROS was acquired on a BD LSRFortessa X-20 flow cytometer (excitation 488 nm, emission 525 nm) and quantified in FlowJo to assess oxidative stress across groups. .. 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). .. After three PBS washes, fluorescent secondary antibodies (Servicebio, Alexa Fluor 488, GB25303; Alexa Fluor 594, GB28303) were incubated for 1 h in the dark, nuclei were counterstained with DAPI (1 μg mL −1 , 5 min, Servicebio, G1012), and images were acquired on a Nikon Eclipse C2 confocal microscope (Japan).



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    Image Search Results


    qPCR primer information.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    doi: 10.3389/fbioe.2026.1924086

    Figure Lengend Snippet: qPCR primer information.

    Article Snippet: The sections were subsequently reacted with primary antibodies targeting COL2A1 (Proteintech, 28459-1-AP), MMP13 (Proteintech, 18165-1-AP), p-PI3K (HUABIO, HA721672), and p-AKT (Proteintech, 66444-1-Ig) for 16 h at 4 °C.

    Techniques: Sequencing

    PGG-Zn@Cur restored matrix metabolic homeostasis in IL-1β-stimulated chondrocytes. (A) Representative immunofluorescence images of COL2A1 in chondrocytes after different treatments. COL2A1 was stained red, and nuclei were counterstained with DAPI. (B) Representative immunofluorescence images of MMP13 in chondrocytes after different treatments. MMP13 was stained green, and nuclei were counterstained with DAPI. (C) Quantitative analysis of relative fluorescence intensity for COL2A1 and MMP13 based on immunofluorescence staining. IL-1β stimulation decreased COL2A1 expression and increased MMP13 accumulation, whereas PGG-Zn@Cur treatment restored COL2A1 fluorescence intensity and suppressed MMP13-positive signals. (D–G) RT-qPCR analysis of cartilage matrix metabolism-related genes, including anabolic markers Col2a1 and Aggrecan, and catabolic markers Mmp13 and Adamts5, in chondrocytes after the indicated treatments. (H) Representative Western blot images of iNOS, COL2A1, MMP13, and ACAN protein expression, together with heatmap-based quantitative analysis of Western blot results across different treatment groups. β-Actin was used as the loading control. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: no significant).

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    doi: 10.3389/fbioe.2026.1924086

    Figure Lengend Snippet: PGG-Zn@Cur restored matrix metabolic homeostasis in IL-1β-stimulated chondrocytes. (A) Representative immunofluorescence images of COL2A1 in chondrocytes after different treatments. COL2A1 was stained red, and nuclei were counterstained with DAPI. (B) Representative immunofluorescence images of MMP13 in chondrocytes after different treatments. MMP13 was stained green, and nuclei were counterstained with DAPI. (C) Quantitative analysis of relative fluorescence intensity for COL2A1 and MMP13 based on immunofluorescence staining. IL-1β stimulation decreased COL2A1 expression and increased MMP13 accumulation, whereas PGG-Zn@Cur treatment restored COL2A1 fluorescence intensity and suppressed MMP13-positive signals. (D–G) RT-qPCR analysis of cartilage matrix metabolism-related genes, including anabolic markers Col2a1 and Aggrecan, and catabolic markers Mmp13 and Adamts5, in chondrocytes after the indicated treatments. (H) Representative Western blot images of iNOS, COL2A1, MMP13, and ACAN protein expression, together with heatmap-based quantitative analysis of Western blot results across different treatment groups. β-Actin was used as the loading control. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: no significant).

    Article Snippet: The sections were subsequently reacted with primary antibodies targeting COL2A1 (Proteintech, 28459-1-AP), MMP13 (Proteintech, 18165-1-AP), p-PI3K (HUABIO, HA721672), and p-AKT (Proteintech, 66444-1-Ig) for 16 h at 4 °C.

    Techniques: Immunofluorescence, Staining, Analysis, Fluorescence, Expressing, Quantitative RT-PCR, Western Blot, Control

    PGG-Zn@Cur attenuated PI3K-AKT activation and apoptosis-associated responses in IL-1β-stimulated chondrocytes. (A) Schematic workflow of RNA sequencing and subsequent experimental validation. (B) Heatmap of representative differentially expressed genes related to cartilage matrix metabolism, inflammation, apoptosis, and PI3K-AKT-associated signaling. (C) Volcano plot showing differentially expressed genes between the indicated groups, with representative genes related to cartilage homeostasis, apoptosis, and PI3K-AKT signaling labeled. (D) GO enrichment analysis of differentially expressed genes, including biological process, cellular component, and molecular function categories. (E) KEGG pathway enrichment analysis, with the PI3K-AKT signaling pathway highlighted as a candidate pathway. (F) Representative immunofluorescence images of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 in chondrocytes after different treatments. Nuclei were counterstained with DAPI. (G) Quantitative analysis of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 fluorescence intensity. (H) Representative Western blot images of PI3K-AKT pathway- and apoptosis-related proteins, including p-PI3K, PI3K, p-AKT, AKT, Cleaved-Caspase3, Caspase3, Bax, and BCL2. β-Actin was used as the loading control. (I) Heatmap-based quantitative analysis of Western blot results, summarizing changes in p-PI3K/PI3K, p-AKT/AKT, Cleaved-Caspase3/Caspase3, Bax/β-Actin, and BCL2/β-Actin across different groups. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    doi: 10.3389/fbioe.2026.1924086

    Figure Lengend Snippet: PGG-Zn@Cur attenuated PI3K-AKT activation and apoptosis-associated responses in IL-1β-stimulated chondrocytes. (A) Schematic workflow of RNA sequencing and subsequent experimental validation. (B) Heatmap of representative differentially expressed genes related to cartilage matrix metabolism, inflammation, apoptosis, and PI3K-AKT-associated signaling. (C) Volcano plot showing differentially expressed genes between the indicated groups, with representative genes related to cartilage homeostasis, apoptosis, and PI3K-AKT signaling labeled. (D) GO enrichment analysis of differentially expressed genes, including biological process, cellular component, and molecular function categories. (E) KEGG pathway enrichment analysis, with the PI3K-AKT signaling pathway highlighted as a candidate pathway. (F) Representative immunofluorescence images of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 in chondrocytes after different treatments. Nuclei were counterstained with DAPI. (G) Quantitative analysis of p-PI3K, p-AKT, Cl-Caspase3, and COL2A1 fluorescence intensity. (H) Representative Western blot images of PI3K-AKT pathway- and apoptosis-related proteins, including p-PI3K, PI3K, p-AKT, AKT, Cleaved-Caspase3, Caspase3, Bax, and BCL2. β-Actin was used as the loading control. (I) Heatmap-based quantitative analysis of Western blot results, summarizing changes in p-PI3K/PI3K, p-AKT/AKT, Cleaved-Caspase3/Caspase3, Bax/β-Actin, and BCL2/β-Actin across different groups. ( n = 3, Scale bar: 10 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Article Snippet: The sections were subsequently reacted with primary antibodies targeting COL2A1 (Proteintech, 28459-1-AP), MMP13 (Proteintech, 18165-1-AP), p-PI3K (HUABIO, HA721672), and p-AKT (Proteintech, 66444-1-Ig) for 16 h at 4 °C.

    Techniques: Activation Assay, RNA Sequencing, Biomarker Discovery, Labeling, Analysis, Immunofluorescence, Fluorescence, Western Blot, Control

    PGG-Zn@Cur attenuates OA-associated cartilage degeneration and preserves matrix homeostasis in vivo . (A) Representative Safranin O/Fast Green staining images of knee joint cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. (B) Representative immunofluorescence images of COL2A1 and MMP13 in articular cartilage from different groups. Nuclei were counterstained with DAPI. (C, D) Quantitative analysis of cartilage degeneration using OARSI scores and modified Mankin’s scores. (E) Quantitative analysis of COL2A1 and MMP13 fluorescence intensity in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    doi: 10.3389/fbioe.2026.1924086

    Figure Lengend Snippet: PGG-Zn@Cur attenuates OA-associated cartilage degeneration and preserves matrix homeostasis in vivo . (A) Representative Safranin O/Fast Green staining images of knee joint cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. (B) Representative immunofluorescence images of COL2A1 and MMP13 in articular cartilage from different groups. Nuclei were counterstained with DAPI. (C, D) Quantitative analysis of cartilage degeneration using OARSI scores and modified Mankin’s scores. (E) Quantitative analysis of COL2A1 and MMP13 fluorescence intensity in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Article Snippet: The sections were subsequently reacted with primary antibodies targeting COL2A1 (Proteintech, 28459-1-AP), MMP13 (Proteintech, 18165-1-AP), p-PI3K (HUABIO, HA721672), and p-AKT (Proteintech, 66444-1-Ig) for 16 h at 4 °C.

    Techniques: In Vivo, Staining, Immunofluorescence, Analysis, Modification, Fluorescence

    PGG-Zn@Cur attenuates PI3K-AKT pathway activation and apoptosis-associated cartilage damage in vivo . (A) Representative immunofluorescence images of p-PI3K, p-AKT, and COL2A1 in articular cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. Nuclei were counterstained with DAPI. (B) Representative TUNEL staining images of articular cartilage from different groups. (C) Quantitative analysis of p-PI3K, p-AKT, and COL2A1 fluorescence intensity in articular cartilage. (D) Quantitative analysis of TUNEL-positive chondrocytes in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: pH-responsive Zn 2+ -coordinated gellan gum/γ-polyglutamic acid hydrogel microspheres as functional biomaterials for intra-articular delivery: physicochemical design, smart release, and chondroprotective performance in osteoarthritis

    doi: 10.3389/fbioe.2026.1924086

    Figure Lengend Snippet: PGG-Zn@Cur attenuates PI3K-AKT pathway activation and apoptosis-associated cartilage damage in vivo . (A) Representative immunofluorescence images of p-PI3K, p-AKT, and COL2A1 in articular cartilage from the Sham, OA, OA+ PGG-Zn, OA+ Cur, and OA+ PGG-Zn@Cur groups. Nuclei were counterstained with DAPI. (B) Representative TUNEL staining images of articular cartilage from different groups. (C) Quantitative analysis of p-PI3K, p-AKT, and COL2A1 fluorescence intensity in articular cartilage. (D) Quantitative analysis of TUNEL-positive chondrocytes in articular cartilage. ( n = 5 mice per group, Scale bar: 50 μm *: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001; ns: not significant).

    Article Snippet: The sections were subsequently reacted with primary antibodies targeting COL2A1 (Proteintech, 28459-1-AP), MMP13 (Proteintech, 18165-1-AP), p-PI3K (HUABIO, HA721672), and p-AKT (Proteintech, 66444-1-Ig) for 16 h at 4 °C.

    Techniques: Activation Assay, In Vivo, Immunofluorescence, TUNEL Assay, Staining, Analysis, Fluorescence

    A qPCR analysis of COL2a1 , MMP13 , and iNOS gene expression levels ( n = 4, biological replicates per group). B – D Schematic illustration and representative immunofluorescence images of COL2A1, MMP13, and iNOS, with corresponding quantitative analysis, scale bar = 50 μm ( n = 3, biological replicates per group). Created in BioRender. Huang, K. ( https://BioRender.com/nqgl3ax ). E , F Western blot analysis of COL2A1, MMP13, and iNOS protein levels, with relative quantitative analysis ( n = 3, biological replicates per group). G , H Safranin O and Alcian blue staining of OA chondrocytes treated with different exosomal formulations, with related quantitative analysis, scale bar = 200 μm ( n = 3, biological replicates per group). Data are presented as the mean ± SD. P values are from one-way analysis of variance (ANOVA) with Tukey’s multiple comparisons test ( A , D , F , H ). Data in ( C , E , G ) are representative of three independent experiments with similar results. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Hybrid exosomal nanomotors convert pathological ROS into transport-driving cues to enhance cartilage accumulation in osteoarthritis

    doi: 10.1038/s41467-026-76949-8

    Figure Lengend Snippet: A qPCR analysis of COL2a1 , MMP13 , and iNOS gene expression levels ( n = 4, biological replicates per group). B – D Schematic illustration and representative immunofluorescence images of COL2A1, MMP13, and iNOS, with corresponding quantitative analysis, scale bar = 50 μm ( n = 3, biological replicates per group). Created in BioRender. Huang, K. ( https://BioRender.com/nqgl3ax ). E , F Western blot analysis of COL2A1, MMP13, and iNOS protein levels, with relative quantitative analysis ( n = 3, biological replicates per group). G , H Safranin O and Alcian blue staining of OA chondrocytes treated with different exosomal formulations, with related quantitative analysis, scale bar = 200 μm ( n = 3, biological replicates per group). Data are presented as the mean ± SD. P values are from one-way analysis of variance (ANOVA) with Tukey’s multiple comparisons test ( A , D , F , H ). Data in ( C , E , G ) are representative of three independent experiments with similar results. Source data are provided as a Source Data file.

    Article Snippet: Primary antibodies against ALIX, TSG101, CD81, Calnexin, COL2A1, MMP13, iNOS, Prdx5, Gpx4, Ndufa8, Cox4i1, Traf6, Ikbkg, GAPDH, and VDAC1, used for western blotting, immunofluorescence, and immunohistochemistry, were obtained from Abclonal, China.

    Techniques: Analysis, Gene Expression, Immunofluorescence, Western Blot, Staining

    A – C Representative histological staining of the affected OA joint treated with different exosomal formulations, including Hematoxylin & Eosin ( A ), Safranin O & Fast Green ( B ), and Toluidine Blue ( C ), scale bar = 200 μm. D – F Quantitative analysis of cartilage thickness ( D ), chondrocyte number ( E ), and OARSI score ( F ) ( n = 4, biological replicates per group). G – I Representative immunohistochemical staining of COL2A1 ( G ), MMP13 ( H ), and iNOS ( I ) in cartilage tissues, scale bar = 200 μm. J – L Quantitative analysis of immunohistochemical expression of COL2A1 ( J ), MMP13 ( K ), and iNOS ( L ) ( n = 4, biological replicates per group). Data are presented as the mean ± SD. P values are from one-way analysis of variance (ANOVA) with Tukey’s multiple comparisons test ( D – E , J – L ), or non-parametric tests (Kruskal-Wallis followed by two-tailed Mann-Whitney U test) ( F ). Data in ( A – C , G – I ) are representative of four independent experiments with similar results. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Hybrid exosomal nanomotors convert pathological ROS into transport-driving cues to enhance cartilage accumulation in osteoarthritis

    doi: 10.1038/s41467-026-76949-8

    Figure Lengend Snippet: A – C Representative histological staining of the affected OA joint treated with different exosomal formulations, including Hematoxylin & Eosin ( A ), Safranin O & Fast Green ( B ), and Toluidine Blue ( C ), scale bar = 200 μm. D – F Quantitative analysis of cartilage thickness ( D ), chondrocyte number ( E ), and OARSI score ( F ) ( n = 4, biological replicates per group). G – I Representative immunohistochemical staining of COL2A1 ( G ), MMP13 ( H ), and iNOS ( I ) in cartilage tissues, scale bar = 200 μm. J – L Quantitative analysis of immunohistochemical expression of COL2A1 ( J ), MMP13 ( K ), and iNOS ( L ) ( n = 4, biological replicates per group). Data are presented as the mean ± SD. P values are from one-way analysis of variance (ANOVA) with Tukey’s multiple comparisons test ( D – E , J – L ), or non-parametric tests (Kruskal-Wallis followed by two-tailed Mann-Whitney U test) ( F ). Data in ( A – C , G – I ) are representative of four independent experiments with similar results. Source data are provided as a Source Data file.

    Article Snippet: Primary antibodies against ALIX, TSG101, CD81, Calnexin, COL2A1, MMP13, iNOS, Prdx5, Gpx4, Ndufa8, Cox4i1, Traf6, Ikbkg, GAPDH, and VDAC1, used for western blotting, immunofluorescence, and immunohistochemistry, were obtained from Abclonal, China.

    Techniques: Staining, Analysis, Immunohistochemical staining, Expressing, Two Tailed Test, MANN-WHITNEY

    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