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电针通过改善脑源性神经营养因子介导的脑缺血再灌注损伤大鼠海马突触可塑性来减轻认知障碍。

Electro-acupuncture ameliorates cognitive impairment via improvement of brain-derived neurotropic factor-mediated hippocampal synaptic plasticity in cerebral ischemia-reperfusion injured rats.

作者信息

Lin Ruhui, Li Xiaojie, Liu Weilin, Chen Wenlie, Yu Kunqiang, Zhao Congkuai, Huang Jia, Yang Shanli, Peng Hongwei, Tao Jing, Chen Lidian

机构信息

Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

Fujian Rehabilitation Tech Co-innovation Center, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.

出版信息

Exp Ther Med. 2017 Sep;14(3):2373-2379. doi: 10.3892/etm.2017.4750. Epub 2017 Jul 10.

Abstract

A previous study by our group found that electro-acupuncture (EA) at the Shenting (DU24) and Baihui (DU20) acupoints ameliorates cognitive impairment in rats with cerebral ischemia-reperfusion (I/R) injury. However, the precise mechanism of action has remained largely unknown. The present study investigated whether brain-derived neurotropic factor (BDNF) mediates hippocampal synaptic plasticity as the underlying mechanism. Rats were randomly divided into three groups: The sham operation control (Sham) group, the focal cerebral ischemia-reperfusion (I/R) group, and the I/R with EA treatment (I/R+EA) group. The I/R+EA group received EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints after the operation. EA treatment was found to ameliorate neurological deficits (P<0.05) and reduce the cerebral infarct volume (P<0.01). In addition, EA improved cognitive function in cerebral I/R-injured rats (P<0.05). Furthermore, EA treatment promoted synaptic plasticity. Simultaneously, EA increased the hippocampal expression of BDNF, its high-affinity tropomyosin receptor kinase B (TrkB) and post-synaptic density protein-95 (PSD-95) in the rats with cerebral I/R injury. Collectively, the findings suggested that BDNF-mediated hippocampal synaptic plasticity may be one mechanism via which EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints improves cognitive function in cerebral I/R injured rats.

摘要

我们团队之前的一项研究发现,针刺神庭穴(督脉24)和百会穴(督脉20)可改善脑缺血再灌注(I/R)损伤大鼠的认知障碍。然而,其确切作用机制在很大程度上仍不清楚。本研究调查了脑源性神经营养因子(BDNF)是否作为潜在机制介导海马突触可塑性。将大鼠随机分为三组:假手术对照组(Sham)、局灶性脑缺血再灌注(I/R)组和I/R+电针治疗组(I/R+EA)。I/R+EA组术后在神庭穴(督脉24)和百会穴(督脉20)接受电针治疗。结果发现,电针治疗可改善神经功能缺损(P<0.05),并减少脑梗死体积(P<0.01)。此外,电针改善了脑I/R损伤大鼠的认知功能(P<0.05)。此外,电针治疗促进了突触可塑性。同时,电针增加了脑I/R损伤大鼠海马中BDNF、其高亲和力原肌球蛋白受体激酶B(TrkB)和突触后致密蛋白95(PSD-95)的表达。总的来说,这些发现表明,BDNF介导的海马突触可塑性可能是针刺神庭穴(督脉24)和百会穴(督脉20)改善脑I/R损伤大鼠认知功能的一种机制。

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