Asiaticoside ameliorates osteoarthritis progression through activation of Nrf2/HO-1 and inhibition of the NF-κB pathway.

Osteoarthritis has become the fourth cause of disability in the world and its occurrence and development are caused by apoptosis and extracellular matrix (ECM) degradation of chondrocytes. Asiaticoside (ASI) is a triterpene saponin compound obtained from Centella Asiatica and has anti-inflammatory and anti-apoptotic effects in various diseases. However, its effects on OA are not clear. In this study, we reported that ASI has a protective effect on the occurrence and progression of OA in vivo and in vitro, and demonstrated its potential molecular mechanism. In vitro, ASI treatment inhibited the release of pro-apoptotic factors induced by TBHP and promoted the release of the anti-apoptotic proteins. In addition, ASI promotes the expression of Aggrecan and Collagen II, while inhibiting the expression of thrombospondin motifs 5 (ADAMTS5) and matrix metalloproteinase-13 (MMP-13), which causes extracellular matrix (ECM) degradation. Mechanistically, ASI exerts its anti-apoptotic effect by activating the Nrf2/HO-1 pathway and preventing p65 from binding to DNA. Similarly, in vivo, ASI has been shown to have a protective effect in a mouse OA model. The conclusion is that our research shows that ASI can be used as a potential drug for the treatment of OA.