〔Abstract〕 Objective To investigate the role of Taraxasterol(TAR) on ferroptosis in chondrocytes induced by Erastin. Methods The C28/I2 chondrocyte line was treated with Erastin to construct the ferroptosis model of chondrocytes in vitro and the experiments were divided into Control, Erastin, TAR,and TAR + Erastin groups.Cell viability was detected by the CCK-8 assay.Cytotoxicity was detected by the lactate dehydrogenase(LDH) kit and the Calcein/PI cytokinesis kit.Flow cytometry was used to detect lipid reactive oxygen species(ROS).The intracellular glutathione(GSH) content was detected by GSH kit.Mitochondrial membrane potential was detected by JC-1 staining and RH123 staining.ACSL4 and GPX4 protein expression and the key indicators of ferroptosis were detected by Western blot. Results TAR restored the decreased cell viability of C28/I2 chondrocytes induced by Erastin treatment as well as reduced Erastin-induced cytotoxicity(P<0.01).Compared with the control group, the level of intracellular lipid ROS increased(P<0.01) and the content of GSH decreased(P<0.01) after treatment with Erastin, while TAR could reduce the production of lipid ROS(P<0.01) and increase the content of GSH(P<0.01).TAR restored mitochondrial membrane potential in C28/I2 chondrocytes ferroptosis, decreased ACSL4 protein expression(P<0.01) and increased GPX4 protein expression(P<0.01).In addition, TAR restored the reduced cell viability caused by IL-1β treatment. Conclusion TAR can inhibit Erastin induced ferroptosis in C28/I2 chondrocytes, which may be related to the regulation of ACSL4 and GPX4 protein expression.