Osteoarthritis (OA) is a common disease in the elderly and seriously affects the quality of life of patients. Tra2β is a protein that has been found to activate PI3K/Akt in recent years. The purpose of this study was to explore the protective effects of Tra2β on chondrocytes and its mechanisms.
The expression of Tra2β in knee cartilage tissue of patients with OA and normal people was compared. In addition, human primary chondrocytes were cultured, the expression of Tra2β in chondrocytes by cell transfection was changed, and its effects on extracellular matrix, inflammation, and apoptosis in chondrocytes were examined. LY294002 was also used to inhibit the activity of PI3K/Akt signaling pathway to verify the mechanism of Tra2β to protect chondrocytes.
The expression of Tra2β in the cartilage tissue of the OA group was significantly lower than that of the control group, and the IL-1β-induced chondrocytes also expressed the lower Tra2β. The overexpression of Tra2β increased the expression of extracellular matrix collagen II and decreased the expressions of MMP3/13, inflammatory factors (IL-6, IL-8 and TNF-α), and apoptotic factors (caspase3/9, Bax). In addition, the overexpression of Tra2β also increased expression and phosphorylation of PI3K and Akt. However, LY294002 attenuated the protective effect of Tra2β on chondrocytes by inhibiting the PI3K/Akt signaling pathway.
Tra2β activates the PI3K/Akt signaling pathway, reduces the degradation of extracellular matrix of chondrocytes, reduces the level of inflammation and apoptosis of chondrocytes, and thus, plays a role in the treatment of OA.