LRWXG has previously been reported to have a protective effect on chondrocytes, preventing apoptosis induced by oxidative stress. In this study, we were aimed at determining whether LRWXG exerts its anti-apoptotic activity through the MAPK signaling pathways in chondrocytes. Our results show that, at the cellular level, apoptosis of chondrocytes in the groups treated by LRWXG decreases compared with groups treated by inhibitors alone and model group under conditions of oxidative stress in a dose-dependent manner. Mechanistically at the molecular level, LRWXG regulates the MAPK pathway induced by oxidative stress: The levels of phosphorylation of JNK and p38 proteins in the groups treated by LRWXG are lower than model group, while compared with corresponding groups of inhibitors, there are no significant difference; For other related proteins, LRWXG reduces the levels of the apoptosis-related proteins BAX and cleaved caspase-3, and increases the level of anti-apoptotic protein BCL2. In addition, LRWXG can significantly reduce the levels of inflammatory-related factors such as COX2, PEG2, TNFα and IL1β, and inhibits the expression of MMPs, increasing the content of type II collagen. The results of this research strongly suggest that LRWXG exerts its anti-apoptotic activity via regulating the MAPK signaling pathways in vitro.
Keywords: Apoptosis; Lower range of molecular weight of xanthan gum; Mitogen-activated protein kinase.
Copyright © 2019. Published by Elsevier B.V.