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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 effects of dexamethasone on the expressions of autophagy-related factors Beclin1 and LC3 in the rat soleus muscle myocytes (CIM), and to explore the possible mechanism of dexamethasone-induced critically ill myopathy in rats. Methods Healthy SD rats were divided into control group and experimental group. Experimental group was divided into 3 groups at 7, 9 and 11 days (n = 10). The experimental group received 5mg / kg dexamethasone continuous intraperitoneal injection once a day, and the control group received intraperitoneal injection of the same amount of normal saline. Footprint method to determine muscle function defects. Immunohistochemistry and Western blot were used to detect the expression of autophagy-related factors Beclin1 and LC3 in soleus muscle cells. Results Compared with the control group, rats in the experimental group showed different degrees of muscular dysfunction symptoms, and the degree of the defect in the rats was the most serious on the 11th day. The results of Western blot showed that Beclin1 and LC3 were positive in the control group or weakly visible Beclin1 and LC3. The expression of Beclin1 and LC3 was obvious in the experimental group as time went on, and the expression was most obvious at the 11th day. Immunohistochemistry also confirmed the same trend. Conclusion Dexamethasone-induced rat CIM may play an important role in the regulation of autophagy by activating the expression of Beclin1 and LC3.