Enoxolone suppresses apoptosis in chondrocytes and progression of osteoarthritis via modulating the ERK1/2 signaling pathway.

Introduction: Osteoarthritis (OA) is an inflammatory disorder of synovial joints which is mainly treated with therapeutic agents showing side effects associated with the gastrointestinal (GI) and metabolic system. Consequently, there is urgent need for a potent, safe and novel agent for treating OA and related disorders. Enoxolone is a pentacyclic triterpenoid obtained from the herb liquorice. Based on earlier findings, we postulated that enoxolone may produce chondroprotective activity by exerting anti-inflammatory, anti-catabolic and oxidative stress-decreasing effects. Material and methods: The chondrocytes were extracted from the femoral head articular cartilage of healthy rats. Immunofluorescence staining was done for identification of chondrocytes. Cell viability and proliferation studies were done using Cell Counting Kit-8. Apoptotic cells were identified by TUNEL assay and flow cytometry analysis. Autophagy was assessed by monodansylcadaverine assay. Western blot analysis was done for expression of proteins. Results: In the present study we investigated the protective effect of enoxolone on interleukin 1β (IL-1β) treated I Conclusions: Our findings demonstrate that enoxolone could suppress inflammatory signaling and apoptosis via the ERK1/2 pathway in chondrocytes.