Electro-acupuncture at points of Zusanli and Quchi exerts anti-apoptotic effect through the modulation of PI3K/Akt signaling pathway

被引：67

作者：

Xue, Xiehua ^{[1
]}

You, Yongmei ^{[2
]}

Tao, Jing ^{[2
]}

Ye, Xiaoqian ^{[3
]}

Huang, Jia ^{[3
]}

Yang, Shanli ^{[3
]}

Lin, Zhicheng ^{[4
]}

Hong, Zhenfeng ^{[4
]}

Peng, Jun ^{[4
]}

Chen, Lidian ^{[1
]}

机构：

[1] Fujian Univ Tradit Chinese Med, Coll Rehabil Med, Fuzhou 350108, Fujian, Peoples R China

[2] Fujian Univ Tradit Chinese Med, MOE Key Lab Tradit Chinese Med Osteol & Traumatol, Fuzhou 350108, Fujian, Peoples R China

[3] Fujian Univ Tradit Chinese Med, Fujian Key Lab Exercise Rehabil, Fuzhou 350108, Fujian, Peoples R China

[4] Fujian Univ Tradit Chinese Med, Fujian Key Lab Integrat Med Geriatr, Fuzhou 350108, Fujian, Peoples R China

来源：

NEUROSCIENCE LETTERS | 2014年 / 558卷

基金：

中国国家自然科学基金;

关键词：

Electro-acupuncture; Cerebral ischemia-reperfusion; PI3K/Akt; Neuroprutective effect; Apoptosis; REPERFUSION INJURED RATS; CEREBRAL-ISCHEMIA; AKT; ACTIVATION; BAX; EXPRESSION;

D O I：

10.1016/j.neulet.2013.10.029

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We evaluated the neuroprotective effect of electro-acupuncture (EA) on cerebral ischemia-reperfusion (IR) injury and deeply investigated the relationship between this neuroprotective effect and PI3K/Akt pathway. Rats underwent focal cerebral IR injured by suture method and received the in vivo therapeutic efficacy of EA at points of Zusanli(ST36) and Quchi(LI11) after the operation. We found that the EA treatment significantly (p<0.05) improved neurological deficit and cerebral infarction. Furthermore, EA profoundly activated PI3K/Akt signaling resulted in the inhibition of cerebral cell apoptosis in the ischemic penumbra. Simultaneously EA increased the expression of PI3K, p-Akt, p-Bad and Bcl-2 at the protein level and the expression of Bcl-2 at the mRNA level. On the contrary, EA inhibited the Bax and cleaved Caspase-3-positive expression. The selective PI3K inhibitor LY294002 compromised EA-induced neuroprotective effects and reduced the elevation of p-Akt, p-Bad and Bcl-2 levels. Our data suggested that the PI3K/Akt pathway played a critical role in mediating the neuroprotective effects of EA treatment at points of Zusanli and Quchi after the ischemic stroke. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

引用

页码：14 / 19

页数：6

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