Astragaloside IV protects against apoptosis in human degenerative chondrocytes through autophagy activation.

Abstract

Increased cell apoptosis in chondrocytes is a feature of degenerative cartilage. Astragaloside IV (AST) has been proven to possess an antiarthritic effect by preventing interleukin (IL)-1β-induced cartilage damage. However, the role of AST on chondrocyte apoptosis and its underlying mechanism remains unknown. In the present study, degenerative chondrocytes isolated from patients with osteoarthritis (OA) were subjected to AST and IL-1β treatment. Results indicated that AST protected against chondrocyte apoptosis induced by IL-1β. Western blotting indicated that AST increased the protein expression of LC3-II/I and decreased P62/SQSTM1 expression, which suggested that AST upregulated autophagy activity in chondrocytes. Fluorescent protein GFP-LC3 analysis and transmission electron microscopy observation confirmed that autophagy was promoted by AST. In contrast, after autophagy inhibited by 3-methyladenine, chondrocyte apoptosis was further increased under IL-1β treatment. Ultimately, rapamycin was used as a positive control, whose results confirmed that rapamycin-mediated autophagy also decreased chondrocyte apoptosis induced by IL-1β. In conclusion, these results suggested that AST-mediated autophagy serves an anti-apoptotic role in chondrocytes, which may aid the development of novel therapeutic approaches for OA treatment.