Brucine restores sodium nitroprusside-induced chondrocyte dysfunction by suppressing the GSK-3β/β-catenin pathway

The dysfunction of chondrocytes is thought to play a role in the initiation and progression of osteoarthritis (OA). Brucine possesses wide pharmacological activities. But the protective mechanism of the brucine on chondrocytes remains unclear. This study is aimed to determine the therapeutic effects of brucine on the mouse chondrocyte OA model by sodium nitroprusside (SNP). The primary chondrocytes were obtained from the knee articular cartilage of a healthy suckling mouse donor. The cultured chondrocytes were divided into the control group, SNP group, brucine group, brucine-SNP group, brucine-SNP-GSK-3β antagonist group (brucine-SNP^- group), and brucine-SNP-GSK-3β agonist group (brucine-SNP-GSK-3β⁺ group). After 24 h, the chondrocytes from different treated groups were collected to detect chondrocyte proliferation and ultrastructure, regulation factors, apoptosis, oxidative stress, and GSK-3β/β-catenin pathway. Compared to the SNP group, chondrocyte proliferation, and regulation factors were promoted, and chondrocyte apoptosis, oxidative stress, and the GSK-3β/β-catenin pathway were inhibited by brucine. It indicates that the adverse effect of SNP is reversed by the brucine on the chondrocyte. Compared to the brucine-SNP group, the effect of brucine on the chondrocyte proliferation, regulation factothe apoptosis, and oxidative stress were promoted by the GSK-3β antagonist. It indicates that the chondrocyte is protected agairucine through buying the GSK-3β/β-catenin pathway.