【摘要】：目的觀察地塞米松對大鼠危重病性肌病(CIM)比目魚肌細胞自噬相關(guān)因子Beclin1和LC3表達的影響,探討地塞米松誘導的大鼠危重病性肌病的可能機制。方法將健康SD大鼠分為對照組和實驗組;實驗組又分為7,9,11d 3個時相點(n=10)。實驗組采用5mg/kg地塞米松連續(xù)腹腔注射,每天1次,對照組腹腔注射等量的生理鹽水。采用足跡法判定肌功能缺損情況。利用免疫組化和Western blot檢測比目魚肌細胞自噬相關(guān)因子Beclin1和LC3的表達情況。結(jié)果與對照組相比,實驗組大鼠出現(xiàn)不同程度肌肉功能缺損癥狀,以11d時大鼠缺損程度最為嚴重。Western blot結(jié)果顯示,對照組或可見微弱的Beclin1、LC3陽性表達,隨著時間延長,實驗組可見明顯的Beclin1、LC3陽性表達,以11d時相點表達最為明顯。免疫組化結(jié)果也證實了同一趨勢。結(jié)論地塞米松誘導的大鼠CIM可能通過激活Beclin1和LC3的表達從而發(fā)揮對細胞自噬的調(diào)節(jié)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.
【作者單位】： 錦州醫(yī)科大學解剖學教研室;錦州禾豐牧業(yè)有限公司;
【基金】：國家自然科學基金(31170930)
【分類號】：R965

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