RORC抑制剂可通过抑制IL-17减弱骨性关节炎细胞凋亡

RORC Inhibitor Attenuates the Apoptosis of Osteoarthritis Cells by Suppressing IL-17

目的探讨维甲酸相关孤儿核受体C(retinoic acid receptor related orphan C,RORC)在骨性关节中的功能及机制。方法建立确乙酸钠(monosodium iodoacetate,MIA)诱导的骨性关节炎(osteoarthritis,OA)细胞模型,采用qRT-PCR检测RORC mRNA的表达,MTT法检测细胞活力,Armexin V-FITC/PI Apoptosis Detection kit、Western印迹及Caspase-3活力检测试剂盒测定OA软骨细胞调亡率及调亡相关蛋白的表达与活力,ELISA试剂盒检测IL-17与炎性因子的表达。结果在OA模型中R0RC的蛋白及mRNA表达水平升高,SR1001(RORC抑制剂)可使OA细胞模型细胞活力上调,细胞凋亡率显著降低,并抑制IL-17及炎性因子IL-6、IL-8、TNF-α的释放。过表达IL-17可减弱SR1001对OA模型凋亡的抑制作用。结论R0RC抑制剂可通过减少IL-17的释放,保护软骨细胞,抑制骨性关节炎。

Objective To investigate the function and mechanism of retinoic acid receptor related orphan C(RORG)in osteoarthritis(OA).Methods The monosodium iodoacetate(MIA)-induced OA model was established in this study.The expression of RORC mRNA was detected by qRT-PCR.Cell viability was measured by MTT.The cell apoptosis rate of the OA model was examined by Annexin V-FITC/PI Apoptosis Detection Kit.The expression and activity of apoptosis-related proteins were detected by Western blot and Caspase-3 Activity Assay Kit.The levels of IL-17 and inflammatory factors were measured by ELISA Kit.Results The expression of RORC mRNA and protein was up-regulated in the OA cell model.The RORC inhibitor SR 1001 promoted the cell viability,and inhibited the apoptosis and release of IL-17 and inflammatory factors in the OA cell model.Over-expressing IL-17 attenuated the suppressed effect of SR 1001 on cell apoptosis in the OA model.Conclusion RORC inhibitors can protect cartilage cells and inhibit osteoarthritis by reducing the release of IL-17.