Role of phosphoinositide 3-kinase/AKT signaling pathway in promoting angiogenesis in rats with focal cerebral ischemia/reperfusion using electrical acupuncture

张珊珊; 罗勇; 武磊

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Role of phosphoinositide 3-kinase/AKT signaling pathway in promoting angiogenesis in rats with focal cerebral ischemia/reperfusion using electrical acupuncture

更新时间：2026-01-09

- Role of phosphoinositide 3-kinase/AKT signaling pathway in promoting angiogenesis in rats with focal cerebral ischemia/reperfusion using electrical acupuncture
- Journal of Army Medical University Vol. 32, Issue 23, Pages: 2488-2491(2010)
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  CLC： R743.31;R364.33;R394.2
- Published：2010
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张珊珊,罗勇,武磊.PI3K/AKT通路在电针促进局灶脑缺血再灌注大鼠脑内血管再生中的作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2488-2491.

　Zhang Shanshan,Luo Yong,Wu Lei.Role of phosphoinositide 3-kinase/AKT signaling pathway in promoting angiogenesis in rats with focal cerebral ischemia/reperfusion using electrical acupuncture[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2488-2491.
张珊珊,罗勇,武磊.PI3K/AKT通路在电针促进局灶脑缺血再灌注大鼠脑内血管再生中的作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2488-2491. DOI：

　Zhang Shanshan,Luo Yong,Wu Lei.Role of phosphoinositide 3-kinase/AKT signaling pathway in promoting angiogenesis in rats with focal cerebral ischemia/reperfusion using electrical acupuncture[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2488-2491. DOI：

摘要

目的观察电针对PI3K/AKT信号转导通路激活的影响，探讨电针促进脑内缺血区血管再生的可能机制。方法采用线栓法制备SD大鼠局灶脑缺血再灌注模型。取双侧“合谷”穴（LI 4）为电针穴位，将80只SD大鼠完全随机分为正常组（n=10）、模型组（n=30）、电针组（n=30）、电针+LY294002组（n=10）。模型组和电针组分别包括再灌注1、3、7 d 3个时相点，每个时相点10只。采用免疫组化法检测各时间点大脑缺血半影区p-AKT1、AC133蛋白的表达；逆转录聚合酶链法检测AC133 mRNA的表达；免疫印迹法定量检测总AKT1、p-AKT1蛋白的表达。结果与正常组比较，模型组和电针组大鼠脑缺血组织p-AKT1蛋白表达增加（P0.05），AKT1蛋白表达无明显差异（P0.05），AC133蛋白和mRNA 表达增加（P0.05）。与模型组比较，电针组p-AKT1蛋白表达于再灌注3、7 d有明显增高（P0.05），再灌注3、7 d AC133蛋白和mRNA表达增加（P0.05）。在PI3K/AKT信号转导通路特异性阻断剂LY294002作用下，大鼠p-AKT1蛋白的表达较电针组显著减少（P0.05），AC133蛋白表达阴性，AC133 mRNA表达减少，与正常组比较无明显差异（P0.05）。结论电针可能加强PI3K/AKT信号转导通路的激活，促进EPCs归巢至缺血组织区，从而促进血管再生。

Abstract

Objective To study the role of electrical acupuncture (EA) in activating the PI3K/AKT signaling pathway and its mechanism underlying the angiogenesis in rats with focal cerebral ischemia/reperfusion. Methods A focal cerebral ischemia/reperfusion model was established by filament occlusion. Heku point (LI 4) was selected for electrical acupuncture. Eighty SD rats were randomly divided into control group（n=10）

model group（n=30）

EA group （n=30）

and EA+LY294002 group（n=10）. Rats in model and EA groups accepted reperfusion on days 1

3 and 7. Expression of p-AKT1 and AC133 was detected by immunohistochemistry （IHC）. Expression of AC133 mRNA was detected by PCR. Expression of p-AKT1 and AKT1 was detected by Western blotting. Results The expression level of p-AKT1

AC133 and AC133 mRNA was higher in model and EA groups than in control group（P0.05）with no significant difference in expression of AKT1 between the 2 groups. The expression level of p-AKT1

AC133 and AC133 mRNA was significantly higher in EA group than in control group in 3 and 7 d after reperfusion（P0.05）. The expression level of p-AKT1

AC133 and AC133 mRNA was significantly lower in EA+LY294002 group than in EA group （P0.05）

with no difference between EA+LY294002 group and control group. Conclusion EA can activate the PI3K/AKT signaling pathway

promote EPC homing to the ischemic zone

and thus lead to angiogenesis.

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