Abstract

Multiple studies have suggested that long non-coding RNAs (lncRNAs) are involved in the development and progression of osteoarthritis (OA). However, how lncRNA SNHG1 regulates OA remains unknown. This study aimed to explore how SNHG1 regulates chondrocyte apoptosis and inflammation. Our data showed that H 2 O 2 -treated chondrocytes exhibited lower expression of SNHG1 and secreted higher levels of IL-6, IL-8, and TNF-α than untreated cells. Further, overexpressing SNHG1 reduced chondrocyte apoptosis and production of inflammatory factors. Additionally, SNHG1 targets miR-195 directly, and IKK-α has direct biding sites for miR-195. Of note, IKK-α acts as an inhibitor of the NF-κB signaling pathway. These findings suggest that SNHG1 can upregulate IKK-α by inhibiting miR-195 and thus, inhibit NF-κB activity. Our in vivo experiments validate our in vitro findings. Thus, under oxidative stress, SNHG1 inhibits the activation of NF-κB to attenuate chondrocyte apoptosis and inflammation via the miR-195/IKK-α axis. Targeting SNHG1 may serve as a potential novel therapeutic approach for OA.