MMP13 Antibody - #AF5355

Fig. 7: Functional and mechanistic insights of AAT-ZCG for DM bone defects in regulating FoxO1/P53 signaling pathways. A Volcano plot showing differentially expressed genes (DEGs) between experimental and control groups. Red dots indicate up-regulated genes, and blue dots indicate down-regulated genes. B Gene Ontology (GO) enrichment analysis of up-regulated genes. C GO enrichment analysis of down-regulated genes. D Heatmap of the expression levels of DEGs across experimental groups, with specific key genes like FoxO1 highlighted. E Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis of DEGs, identifying significant pathways such as P53 signaling, FoxO1 signaling. F Schematic diagram illustrates the proposed mechanism of AAT-ZCG in activating the forkhead box O1 (FoxO1) and P53 pathways. G Western blot was conducted to evaluate the effects of AAT-ZCG on inflammation and osteogenesis through the FoxO1/P53 signaling pathway. H The effect of AAT-ZCG on the expression of FoxO1, n = 3. I The effect of AAT-ZCG on P53 expression, n = 3. J The effect of AAT-ZCG on the expression of pP53, n = 3. K The effect of AAT-ZCG on the expression of MMP13, n = 3. L The effect of AAT-ZCG on the expression of BMP2, n = 3. M) The effect of AAT-ZCG on the expression of Acp5, n = 3. Data are presented as mean ± SD. Figure 7H-M involved three biological replications (n = 3) and analysis of these experiments’ results were performed using one-way ANOVA. ns, no statistical significance. Statistical significance is indicated as follows: P 

Fig. 4. Stressed-relaxed HAMA@Lip exhibits good biocompatibility and alleviates chondrocyte ERS and OA phenotypes. (A) CCK-8 assay results for chondrocytes treated with blank, Lip, stress-relaxed HAMA, and stress-relaxed HAMA@Lip on days 1, 2, and 3 (Blank, Lipo-Wyrgrl@TUDCA; Stress-relaxed HAMA; Stress-relaxed HAMA@Lipo). (B) Cell growth curves under different concentrations of tunicamycin. (C and D) ThT staining results and corresponding fluorescence quantification for different treatment groups (n = 3). (E and F) Col II staining results and corresponding fluorescence quantification for different treatment groups (n = 3). (G and H) Aggrecan staining results and corresponding fluorescence quantification for different treatment groups (n = 3). (I and J) MMP13 staining results and corresponding fluorescence quantification for different treatment groups (n = 3). One-way ANOVA with Tukey’s post hoc test. ns: no significance, *P < 0.05, **P < 0.01.

Fig. 2 PTX3 accelerates synovitis, cartilage erosion, and exacerbates OA development in mice. A, B Safranin O/fast green staining and Osteoarthritis Research Society International (OARSI) grades of knee cartilage from DMM mice treated with vehicle, recombinant mouse PTX3 (rmPTX3), or PTX3 neutralizing antibody (PTX3-NAb) for 4 weeks and 8 weeks. Scale bar: 100 µm. C–F IF staining and quantification of ADATMS5 and MMP13 in knee cartilage of controls and DMM mice treated with vehicle, rmPTX3, or PTX3-NAb for 8 weeks. Scale bar: 50 µm. G IF staining and quantification of COL2 in knee cartilage of controls and DMM mice treated with rmPTX3 or PTX3-NAb for 8 weeks. Scale bar: 50 µm. H, I H&E and synovitis score of synovial tissues from DMM mice treated with vehicle, rmPTX3, or PTX3-NAb for 4 weeks and 8 weeks. Scale bar: 100 µm. *P