应用细胞模型探讨TAZ激活剂对肌萎缩的作用

Effect of TAZ activator on glucocorticoid-induced C2C12 myotube atrophy

目的应用糖皮质激素致C2C12细胞肌管形成萎缩模型,探讨TAZ激活剂对肌萎缩的治疗作用。方法 C2C12细胞按分化培养液中的不同处理分为对照组、地塞米松处理组和地塞米松联合不同浓度IBS008738处理组,荧光显微镜下观察分化后肌管并行免疫染色,用Image J软件测量其直径并计算融合指数。用Real time PCR及Western blot法分析肌萎缩标记基因Mu RF1及Atrogin-1的m RNA及蛋白表达水平。结果IBS008738显著地抵抗地塞米松所致肌管直径及融合指数的减低,下调萎缩相关基因的表达,且其作用有剂量依存性。结论 IBS008738对糖皮质激素肌萎缩有潜在治疗价值。

Objective To investigate the effect of TAZ activator on glucocorticoid-induced C2C 12 myotube atrophy. Methods C2C12 cells were treated by control, dexamethasone with or without IBS008738, observed under the fluorescence microscope and immunostained, myotube diameter and fusion index were measured by using Image J software, and the expression of MuRFland Atrogin-1 were analyzed by Real time PCR and Western blot methods. Results IBS008738 rescued the dexamethasone-indneed reduction of myotube diameter and fusion index, downregulated the expression levels of MuRF1 and Atrogin-1 in a dose-dependent pattern. Conclusion IBS008738 is a potential drug therapy for glucocorticoid-induced atrophy.