Myostatin在地塞米松致肌原纤维损伤中的作用研究

为阐明Myostatin在肌原纤维损伤中的作用,并探讨提高畜禽肉产(质)量或控制人类肌肉萎缩的方法,本试验以小鼠为模式动物,采用高剂量地塞米松构建了严重应激模型,研究生理剂量胰岛素对地塞米松致肌原纤维损伤的影响及其与Myostatin基因表达的关系,以及Myostatin基因免疫对地塞米松致肌原纤维损伤的干预作用.结果表明:地塞米松诱导Myostatin基因表达上调及严重的肌原纤维损伤和线粒体肿胀,而胰岛素注射明显减弱了这些效应；Myostatin基因免疫明显抑制了地塞米松对肌原纤维和线粒体的损伤作用.试验结果提示,Myostatin是参与肌原纤维降解的一个关键因子,该作用可能与其刺激了线粒体的功能有关.

Research on the Role of Myostatin in Dexamethasone-induced Myofibril Damage

In order to clarify the roles of myostatin in myofibril damage and investigate the measures to improve the production and quality of muscle mass in livestock or control the muscle atrophy in human,the serious stress models of mice were made with high-dose dexamethasone,and the effect of physiological-dose insulin on the dexamethasone-induced myofibril damage and the relationship between the effect and myostatin expression were researched.In addition,the intervention effect of myostatin gene immunization on the dexamethasone-induced myofibril damage was studied.The results showed that: dexamethasone upregulated the expression of myostatin gene and caused the serious damage of myofibril and swelling of mitochondria,while insulin attenuated the effects of dexamethasone;myostatin gene immunization reduced the myofibril and mitochondria damages induced by dexamethasone.The results suggest that myostatin is one of key factors for myofibril degradation and the role of myostatin may be attributed to the stimulation of mitochondrial function by myostatin.