ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

The A20‐binding inhibitor of nuclear factor (NF)‐κB‐1 (ABIN‐1) protein has recently been implicated as a key regulator of inflammation with involvement in multiple inflammatory diseases. However, the function of ABIN‐1 in osteoarthritis (OA) remains unclear. In the current study, we explored the role of ABIN‐1 in the regulation of lipopolysaccharide (LPS)‐induced inflammatory injury of chondrocytes, which served as an in vitro model of OA. Results revealed that ABIN‐1 expression was induced by chondrocyte exposure to LPS. ABN‐1 silencing exacerbated LPS‐induced apoptosis and the inflammatory response, while ABIN‐1 overexpression alleviated the inflammatory response and LPS‐induced apoptosis in chondrocytes. Moreover, ABIN‐1 overexpression resulted in significantly decreased LPS‐induced NF‐κB activation. Notably, activation of NF‐κB signalling significantly reversed ABIN‐1‐mediated inhibitory effects on LPS‐induced inflammatory injury in chondrocytes. Taken together, these results demonstrate that ABIN‐1 protects chondrocytes against LPS‐induced inflammatory injury through the suppression of NF‐κB signalling. Our study suggests a potential role for ABIN‐1 in OA. Further, we show that ABIN‐1 may serve as a potential target for controlling joint inflammation.