电针抑制局灶性脑缺血损伤大鼠皮质细胞自噬的实验研究

关键词：电针  神经细胞  自噬  LC3B  PI3K-mTOR  脑缺血性损伤  脑卒中

Keywords:electroacupuncture  neural cell  autophagy  LC3B  PI3K-mTOR  cerebral ischemic injury  stroke

摘要：

      摘要 目的：观察电针“曲池”、“足三里”穴对缺血再灌注（MCAO）大鼠皮质神经细胞PI3K-mTOR信号通路的影响。 方法：参考Koizumi线栓法构建MCAO大鼠模型，电针“曲池”、“足三里”穴干预后，TTC染色观察梗死体积，采用Western blot检测细胞自噬标志蛋白Atg4、LC3B，以及自噬相关信号分子PI3K、mTOR蛋白的表达水平。 结果：TTC染色显示电针减少了MCAO大鼠脑梗死体积；电针抑制了LC3BⅠ向LC3BⅡ的转化；与模型组相比，电针组Atg4表达下降，而PI3K和mTOR蛋白表达水平升高。 结论：电针“曲池”、“足三里”治疗3天抑制细胞自噬相关分子，其可能机制电针激活了PI3K-mTOR信号分子。

Abstract:

      Abstract Objective: To observe effects of electroacupuncture (EA) of "Quchi (LI11)" point, "Zusanli (ST36)" point on the structure of cortical mitochondria and autophagosome in cerebral ischemia reperfusion (MCAO) rats. Method: The model MCAO rats were constructed according to Koizumi methods. After EA at "Quchi", "Zusanli" point intervention, the volumes of cerebral ischemia were observed by TTC staining, electron microscope was used to observe the autophagosome and the structure of mitochondria. Western blot was used to detect autophagy marker protein expression levels of Atg4 and LC3B. Result: TTC staining showed that EA reduced cerebral infarct volumes of rats in model MCAO group. EA intervention inhibited the transformation of LC3B Ⅰ to LC3B Ⅱ. In addition, compared with model group, in EA group the expression of Atg4 decreased, whereas the expressions of PI3K and mTOR proteins increased. Conclusion: MCAO could promote autophagy occuring in cortical cells, while EA at "Quchi (LI11)", "Zusanli (ST36)" for 3d could inhibit the autophagy, the mechanisms maybe mediate PI3K-mTOR signaling.