地塞米松诱导的危重病性肌病大鼠骨骼肌Beclin1、LC3的表达

Expression of Beclin1 and LC3 in dexamethasone-induced rat critical illness myopathy

目的观察地塞米松对大鼠危重病性肌病(CIM)比目鱼肌细胞自噬相关因子Beclin1和LC3表达的影响,探讨地塞米松诱导的大鼠危重病性肌病的可能机制。方法将健康SD大鼠分为对照组和实验组;实验组又分为7,9,11d 3个时相点(n=10)。实验组采用5mg/kg地塞米松连续腹腔注射,每天1次,对照组腹腔注射等量的生理盐水。采用足迹法判定肌功能缺损情况。利用免疫组化和Western blot检测比目鱼肌细胞自噬相关因子Beclin1和LC3的表达情况。结果与对照组相比,实验组大鼠出现不同程度肌肉功能缺损症状,以11d时大鼠缺损程度最为严重。Western blot结果显示,对照组或可见微弱的Beclin1、LC3阳性表达,随着时间延长,实验组可见明显的Beclin1、LC3阳性表达,以11d时相点表达最为明显。免疫组化结果也证实了同一趋势。结论地塞米松诱导的大鼠CIM可能通过激活Beclin1和LC3的表达从而发挥对细胞自噬的调节作用。

Objective To investigate the expression of critical illness myopathy on autophagy-related factors Beclin1 and LC3 in rat skeletal muscle. Method SD rats were divided into control and experimental groups; Experimental groups were divided into 3 time points, i.e., 7, 9 and 11d（n=10）. Experimental groups underwent intraperitoneal injection of dexamethasone 5 mg/kg once per day, and the healthy control group was injected with normal saline. The muscle function defect was determined by footprint method. The expression of skeletal muscle autophagy-related factors Beclin1 and LC3 was examined by immunohistochemistry and western blot analysis. Results Compared with the control group, rats in the experimental groupdemonstrated muscle function impairment symptoms of varying degrees ,which was most serious at 11d time point. Western blot results showed that Beclin1 and LC3 positive expression in the control group, or Beclin1 and LC3 expression were significantly higher in the experimental group than that in the control group. Immunohistochemistry confirmed the same trend. Conclusion Beclin1 and LC3 may play an important role in cell autophagy of skeletal muscle in critical illness myopathy in rats.