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目的:观察养阴通络方对脑缺血损伤大鼠磷酸化Akt(P-Akt)、蛋白激酶B(Akt)及磷脂酰肌醇3-激酶(PI3K)蛋白表达作用,对其神经保护作用机制进行探讨。方法:在长期激怒法致肝肾阴虚证动物模型基础上,采用大鼠线栓法复制局灶性脑缺血再灌注模型,免疫印迹法检测海马p-Akt(Ser473)、Akt、PI3K蛋白的表达。结果:与模型组比较,养阴通络方16g/kg组大鼠海马Akt蛋白表达增加(P<0.01),p-Akt(Ser473)、PI3K蛋白表达水平有升高趋势。结论:养阴通络方对脑缺血损伤保护作用的机制,可能是通过上调PI3K、Akt的表达,促进Akt的磷酸化。
Objective: To observe the effect of Yangyin Tongluo Prescription on the expression of phosphorylated Akt (P-Akt), Akt and PI3K in rats with cerebral ischemia injury and its neuroprotective effect Mechanism to explore. Methods: The focal cerebral ischemia-reperfusion model was induced by long-term anoxia on the basis of animal model of liver-kidney-yin deficiency. The expressions of p-Akt (Ser473), Akt and PI3K expression. Results: Compared with model group, the expression of Akt protein in hippocampus of Yangyin Tongluo formula group increased (P <0.01) and the expression of p-Akt (Ser473) and PI3K protein increased. Conclusion: The protective mechanism of Yangyin Tongluo Prescription on cerebral ischemia injury may be through up-regulating the expression of PI3K and Akt and promoting the phosphorylation of Akt.