Fig 2: Angptl4 knockdown regulated ECM degradation and inflammation through the SIRTUIN 1/NF-?B pathway. (a, b) Expression level of P65, Lamin B, SIRTUIN 1, and GAPDH in chondrocytes as determined by Western blotting. (c, d) Confirmation of the successful knockdown of SIRTUIN 1 via siRNA. (e, f) The expression level of IL-6, Collagen II, ADAMTS5, MMP3, and MMP13 in chondrocytes as determined with Western blotting. (g, f) Immunofluorescence staining of P65 in chondrocytes after the indicated groups (bar: 10 µm). (i, j) Immunofluorescence staining of Collagen II, MMP13 and IL-6 in chondrocytes as treated above (bar: 20 µm). All data are presented as the mean ± SD (n = 5); ns: no significance, **P < 0.01.

Fig 3: Angptl4 knockdown ameliorated the degradation of ECM, inflammation, and apoptosis by inhibiting NF-?B in vivo. (a, b) The expression of p-P65, MMP13, and IL-6 in mouse cartilage as examined by immunohistochemistry (bar: 20 µm). (c, d) Results of the TUNEL staining assay in mouse cartilage (bar: 50 µm). All data are presented as the mean ± SD (n = 5); ns: no significance, **P < 0.01.

Fig 4: XJS inhibited FGL1/NF-?B/STAT3 positive feedback loop. (A–C) The protein expressions of p65 and STAT3 (n = 3). (D) The mRNA expressions of FGL1 (n = 6). (E, F) The protein expressions of FGL1 (n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Fig 5: S100A9 knockout attenuates inflammatory response in aged mice. (A–C) The interleukin 1ß (IL-1ß), IL-6, and tumor necrosis factor a (TNF-a) levels in the serum of mice in different groups (n = 6). (D) Representative Western blots of Phospho-P38 and P65 in the aortas from mice in different groups. The related statistical results were exhibited in (E) and (F) (n = 6). ns, not significant. *P < 0.05, ***P < 0.001, ****P < 0.0001.