Metformin protects chondrocytes against IL-1β induced injury by regulation of the AMPK/NF-κ B signaling pathway.

Osteoarthritis (OA) is a common joint disorder characterized by degeneration and inflammation of the articular cartilage. The etiology of OA is complex, and there is no effective drug for the treatment currently. Metformin, the first-line drug for type 2 diabetes mellitus, has been reported to play an essential role in a variety of diseases; however, whether it could be used in OA therapy remains unclear. In this study, we used interleukin-1β (IL-1β) to mimic the pathophysiology of OA to explore the function and the underlying mechanism of metformin on OA. In our study, cell viability was measured using cell counting kit-8 assay, expressions of crucial factors involved in the extracellular matrix (ECM) metabolic, proinflammatory response, cell apoptosis, and nuclear factor κ B(NF-κ B) pathway were analyzed using western blot analysis and immunofluorescence staining. We found that metformin increased the proliferation of the cells, alleviated IL-1β-induced ECM metabolic imbalance and proinflammatory cytokine production, and exerted anti-apoptosis activity in ATDC5 cells. Furthermore, the results showed that metformin blocked the NF-κ B pathway in IL-1β-induced ATDC5 cells via activation of AMP-activated protein kinase (AMPK). These results indicated that metformin protected chondrocytes against IL-1β-induced injury, possibly by regulation of the AMPK/NF-κ B signaling pathway. It may have the potential as a novel drug for OA treatment.