PRDX1 overexpression contributes to the protection on chondrocytes from IL-1β-induced apoptosis

Peroxiredoxin 1 (PRDX1) is a member of the peroxiredoxin family, which has been shown to act as an antioxidant, whose main function is to reduce reactive oxygen species in cells. The purpose of this article was to study the effect of PRDX1 overexpression on chondrocyte apoptosis in in vitro model (exposure to IL-1β) and explore its mechanism. PRDX1 overexpression was construed and infected chondrocytes for 24 h prior to the addition of10 μg/l IL-1β to isolated chondrocytes. 10 μM SB203580 was added 30 min prior to the addition of IL-1β to isolated chondrocytes. CCK-8 and flow cytometry assay were used to detect the chondrocytes proliferation, apoptosis and ROS production. Real-time PCR and Western blot were performed for examine the expression of MMP-13, Bcl-2 and Bax, and the activation of p38 was measured by Western blot assay. In the current study, we demonstrated that IL-1β treatment inhibited osteoarthritic chondrocytes proliferation and induced apoptosis and ROS production. IL-1β treatment also increased p-p38/p38, MMP-13 and Bax/Bcl-2 expression. However, p38 inhibitor SB203580 and PRDX1 overexpression both inhibited osteoarthritic chondrocytes apoptosis and decreased ROS production in chondrocytes induced by IL-1β treatment. Furthermore, SB203580 and overexpression of PRDX1 also resulted in an altered expression of proteins associated with apoptosis. Collectively, these results demonstrated that the regulatory effects of PRDX1 can be partially attributed to p38 signaling.