The long non-coding RNA SNHG1 attenuates chondrocyte apoptosis and inflammation via the miR-195/IKK- α axis

This study aimed to explore how SNHG1 regulates chondrocyte apoptosis and inflammation. Our data showed that H2O2-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 findi ngs 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.
Source: Cell and Tissue Banking - Category: Stem Cells Source Type: research