Emodin Attenuates the ECM Degradation and Oxidative Stress of Chondrocytes through the Nrf2/NQO1/HO-1 Pathway to Ameliorate Rat Osteoarthritis

Osteoarthritis (OA) substantially reduces the quality of life elderly. OA therapy remains a challenge since no treatment options for its causes are so far available. Over recent years, researchers have speculated that emodin may represent potential strategy OA. However, it unclear whether mechanism action is associated with inhibition OA-induced oxidative stress. In present study, antioxidant and protective properties against development were investigated both in vitro vivo. vitro, inhibited production reactive oxygen species (ROS) chondrocytes induced by hydrogen peroxide (H2O2) reduced expression matrix metalloproteinase (MMP)3 MMP13 concentration-dependent manner. It was found upregulated Nrf2/NQO1/HO-1 pathway, thereby attenuating effects stress caused rat model posttraumatic anterior cruciate ligament transection (ACLT), extent joint swelling. Emodin attenuated damage cartilage upregulating superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) activity, reducing malondialdehyde (MDA) concentration inhibiting extracellular (ECM) degradation biomarkers oligomeric protein (COMP), C-terminal telopeptide type I collagen (CTX-I) II (CTX-II), damage. summary, study indicates ECM via ameliorating rats.