Objective : To explore the effect of 2-aminoethoxy-diphenyl borate(2-APB) on H2 O2 -induced chondro- cyte apoptosis and its mechanism． Methods : The experiment was divided into control group，H2 O2 group，2-APB group and H2 O2 + 2-APB group．CCK-8 method was used to detect the cell viability of each group ; The effect of 2- APB on the morphological changes of chondrocytes induced by H2 O2 was observed under microscopy ; TUNEL meth- od and flow cytometry were used to detect chondrocyte apoptosis ; Flow cytometry was used to detect Lipid reactive oxygen species ( ROS) ; Western blot was used to detect the protein expressions of Cleaved-PARP，p-PKCα and HIF-1α in H2 O2 -induced cells by 2-APB ; Immunofluorescence was used to detect the fluorescent expression of HIF- 1 α in cells induced by H2 O2 by PKCα inhibitor BIM-1 . Results : 2-APB inhibited H2 O2 -induced apoptosis in chon- drocytes，and the inhibitory effect was the most significant when the concentration of 2-APB was 100 μmol / L (F = 235. 80，P ＜ 0. 01 ) ; 22-APB could inhibit the positive rate of H2 O2 -induced apoptosis of chondrocytes ( F = 114. 80，P＜0. 01) and the level of ROS (F = 52. 99，P＜0. 01) ．and inhibited the expression of Cleaved-PARP (F = 10. 10，P＜0. 05) ，p-PKCα (F = 24. 56，P＜0. 05) and HIF-1α proteins (F = 6. 85，P＜0. 05) ．The PKCα in- hibitor BIM-Ⅰ could inhibit the increase in HIF-1α fluorescence intensity caused by H2 O2． Conclusion 2-APB can inhibit chondrocytes apoptosis induced by H2 O2 through the PKCα/ HIF-1α pathway and thus protect chondro- cytes.

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.