地塞米松诱导的危重病性肌病大鼠骨骼肌Beclin1、LC3的表达

发布时间：2018-08-03 19:19

【摘要】：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。
[Abstract]:Objective to observe the effect of dexamethasone on the expression of autophagy related factors (Beclin1 and LC3) in (CIM) soleus myocytes of rats with critical myopathy and to explore the possible mechanism of dexamethasone induced critical myopathy. Methods healthy SD rats were divided into control group and experimental group. 5mg/kg dexamethasone was continuously injected intraperitoneally once a day in the experimental group and saline was injected intraperitoneally in the control group. The defect of muscle function was determined by footprint method. The expression of autophagy related factors (Beclin1 and LC3) in soleus myocytes was detected by immunohistochemistry and Western blot. Results compared with the control group, the rats in the experimental group showed different degrees of muscle dysfunction symptoms. The results of Western blot showed that the weak expression of Beclin1 + LC3 in the control group was the most serious at the 11th day, and the results showed that the expression of Beclin1 + LC3 in the control group was weaker than that in the control group. The positive expression of Beclin1 + LC3 was observed in the experimental group, especially at the phase point of 11 d. The same trend was confirmed by immunohistochemical results. Conclusion Dexamethasone-induced rat CIM may regulate autophagy by activating the expression of Beclin1 and LC3.
【作者单位】：锦州医科大学解剖学教研室;锦州禾丰牧业有限公司;
【基金】：国家自然科学基金(31170930)
【分类号】：R965

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