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. 2022 Mar 9;10:797855. doi: 10.3389/fcell.2022.797855

FIGURE 5.

FIGURE 5

Expression of inflammation-related markers and immunofluorescence analysis of NF-κB p65 in chondrocytes. (A–D) The relative protein expressions were detected in the control (CG), IL-1β group, IL-1β + irisin (5 ng/ml), and IL-1β + irisin (10 ng/ml) groups. Chondrocytes were preincubated with different concentrations of irisin (0, 5, or 10 ng/ml) and treated with IL-1β (10 ng/ml) for 24 h. The levels of expression of ADAMTS-5 and MMP-13 were increased after treatment with IL-1β, whereas decreased after treatment with irisin. In addition, irisin-treated chondrocytes could partially recover the expression of chondrocyte-specific collagen II. The phosphorylation of PI3K, Akt, and NF-κB p65 was significantly suppressed in the irisin-treated group compared with that in the IL-1β group. (E) Relative mRNA expression of collagen II, ADAMTS-5, and MMP-13. The expression of IL-1β-induced inflammatory genes was inhibited by irisin in a dose-independent manner. (F) Effects of irisin on the nuclear translocation of NF-κB p65. Chondrocytes were immunostained using anti-NF-κB p65 rabbit antibody (green) and visualized under a confocal microcope. Cell nuclei were stained with DAPI (blue). Significant nuclear translocation of NF-κB p65 was detected in chondrocytes stimulated with IL-1β (10 ng/ml). In contrast, irisin intervention could reverse this trend. Data were expressed as the mean ± SEM, *p < 0.05 vs. IL-1β; **p < 0.01 vs. IL-1β; ***p < 0.001 vs. IL-1β. # p < 0.05 vs. CG; ## p < 0.01 vs. CG; ### p < 0.001 vs. CG. n = 3 for each group, means ±95% CI.