Receptor-interacting protein 2 (RIP2) is a key mediator implicated in multiple cellular processes, and its dysregulation has been recently reported in colitis, asthma and other inflammatory diseases. However, the effects of RIP2 on osteoarthritis (OA) and the underlying mechanisms remain unclear. In this study, we found that RIP2 expression was upregulated in human articular cartilage tissues with OA and interleukin-1β (IL-1β)-treated chondrocytes. Knockdown of RIP2 inhibited IL-1β-induced extracellular matrix (ECM) and oxidative stress. Moreover, knockdown of TRAF3 reversed the effects of RIP2 silencing on cartilage degradation and oxidative stress in IL-1β-induced chondrocytes. In addition, p38 mitogen-activated protein kinase (MAPK) activator dehydrocorydalmine chloride (Dc) also reversed the effects of RIP2 silencing on IL-1β-induced chondrocytes. Taken together, our data reveal that RIP2 knockdown inhibits cartilage degradation and oxidative stress in IL-1β-treated chondrocytes by regulating TRAF3 expression and p38 MAPK pathway activation.

受体相互作用蛋白 2 (RIP2) 是涉及多个细胞过程的关键介质，最近在结肠炎、哮喘和其他炎症性疾病中报道了其失调。然而，RIP2 对骨关节炎 (OA) 的影响及其潜在机制尚不清楚。在这项研究中，我们发现 RIP2 表达在具有 OA 和白细胞介素-1β (IL-1β) 处理的软骨细胞的人关节软骨组织中上调。RIP2 的敲低抑制了 IL-1β 诱导的细胞外基质 (ECM) 和氧化应激。此外，敲低 TRAF3 逆转了 RIP2 沉默对 IL-1β 诱导的软骨细胞中软骨降解和氧化应激的影响。此外，p38 丝裂原活化蛋白激酶 (MAPK) 激活剂脱氢紫堇碱氯化物 (Dc) 也逆转了 RIP2 沉默对 IL-1β 诱导的软骨细胞的影响。总之，我们的数据表明，RIP2 敲低通过调节 TRAF3 表达和 p38 MAPK 通路激活来抑制 IL-1β 处理的软骨细胞中的软骨降解和氧化应激。