| Objective To investigate the effect of acacetin (Aca) on chondrocyte differentiation in rats with osteoarthritis (OA) and its mechanism. Methods An OA cell model was constructed by treating rat chondrocytes with IL-1β. The rat chondrocytes were randomly divided into control group, OA group, Aca-L low-dose (Aca-L) group, Aca-H high-dose (Aca-H) group, and Aca-H+Colivelin (JAK/STAT signaling pathway activator) group. CCK-8 was applied to detect cell proliferation. Cell apoptosis was detected with flow cytometry. Alixin blue staining was used to evaluate chondrocyte differentiation. The levels of TNF - α, IL-6, IL-10, CTX-I, and CTX-II in the serum were detected using ELISA. Western blotting was used to detect the expression of SOX9, Aggrecan, Collagen II, MMP-3, MMP-13, p-JAK, p-STAT, JAK, and STAT in chondrocytes. Results Compared with those in the control group, the proliferation rate of chondrocytes, degree of Alizarin blue staining, IL-10 level, and SOX9, Aggrecan, and Collagen II protein expression in OA group decreased. The apoptosis rate, the levels of TNF - α, IL-6, CTX-I, and CTX-II, MMP-3, MMP-13, p-JAK/JAK, and p-STAT/STAT protein expression increased (P<0.05). Compared with those in the OA group, the proliferation rate of chondrocytes, degree of Alizarin blue staining, IL-10 level, SOX9, Aggrecan, and Collagen II protein expression in Aca-L and Aca-H groups increased. The apoptosis rate, the levels of TNF-α, IL-6, CTX-I and CTX-II, MMP-3, MMP-13, p-JAK/JAK, and p-STAT/STAT protein expression decreased (P<0.05). Colivelin was able to reduce the improvement effect of Aca on chondrocyte differentiation in OA rats (P<0.05). Conclusion Aca may reduce inflammation and apoptosis of chondrocytes, and may promote proliferation and differentiation of chondrocytes in OA rats by inhibiting the JAK/STAT signaling pathway. |