Icariin arrests cell cycle progression and induces cell apoptosis through the mitochondrial pathway in human fibroblast-like synoviocytes.

Rheumatoid arthritis (RA) is a highly disabling autoimmune disorder, characterized by the proliferation of Fibroblast-like Synoviocytes (FLSs). Icariin is a prenylated flavonol glycoside extracted from the medical plant Epimedium, which can inhibit the proliferation and migration of FLSs. However, the potential mechanism of icariin to alleviate RA remains unclear. In this study, icariin inhibited the migration and proliferation of FLSs in a concentration-dependent manner, by inducing G2/M phase arrest and apoptosis. Icariin reduced the mitochondrial transmembrane potential, upregulated cytosolic cytochrome c and increased the level of intracellular reactive oxygen species (ROS). In conclusion, icariin inhibited the proliferation of FLSs by interfering with the cell cycle process and inducing cell apoptosis, suggesting its potential use for the treatment of RA.