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.