SPRED2 promotes autophagy and attenuates inflammatory response in IL-1β induced osteoarthritis chondrocytes via regulating the p38 MAPK signaling pathway

Osteoarthritis (OA) is an age-related degenerative disease primarily characterized by articular cartilage degeneration. Many inflammatory mediators are upregulated in OA patients. Mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways play a role in the regulation of inflammatory response. Autophagy appears to exhibit a protective mechanism, and alleviate the symptoms of OA in rats. Dysregulation of SPRED2 is associated with various diseases involving inflammatory response. However, the role of SPRED2 in OA development remains to be investigated. The present work demonstrated that SPRED2 promoted autophagy and attenuated inflammatory response in IL-1β induced osteoarthritis chondrocytes via regulating the p38 MAPK signaling pathway. SPRED2 was downregulated in human knee cartilage tissues of OA patients and in IL-1β-induced chondrocytes. SPRED2 enhanced chondrocyte proliferation and prevented cell apoptosis induced by IL-1β. SPRED2 prevented IL-1β-induced chondrocytes autophagy and inflammatory response in chondrocytes. SPRED2 inhibited the activation of p38 MAPK signaling pathway and ameliorated OA injury of cartilage. Thus, SPRED2 promoted autophagy and inhibited inflammatory response by regulation of p38 MAPK signaling pathway in vivo.