Electroacupuncture protects against cerebral ischemia-reperfusion injury via regulating P2×7R expression

IF 1.9 Q3 CLINICAL NEUROLOGY

Cerebral circulation - cognition and behavior Pub Date : 2025-01-01 DOI:10.1016/j.cccb.2025.100379

Sijia Chen , Ye Zhu , Feihong Lin , Hanming Jiang , Haipeng Liu , Shan Li , Xuliang Huang , Yunchang Mo , Junlu Wang , Qinxue Dai

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Abstract

Background

Ischemic stroke is a serious clinical condition that is challenging to cure; therefore, slowing down the depletion of ATP is crucial to enhancing the tolerance of ischemic tissue through preconditioning. Electroacupuncture (EA) preconditioning induces tolerance to cerebral ischemia; however, the underlying mechanism remains unclear.

Objective

The P2×7 receptor (P2×7R) mediates the stimulation of microglial cells and is involved in the development of cerebral ischemia-reperfusion (I/R) damage. We hypothesized that the protective effect of EA preconditioning is associated with the downregulation of P2×7R expression.

Methods

We performed EA at the "Baihui" and "Fengfu" for 30 min before establishing a rat model of cerebral I/R induced based on the middle cerebral artery occlusion model (MCAO). MCAO rats were administered a ventricular injection of 2 '(3′)-O-(4-benzoyl) adenosine triphosphate (BzATP), a P2×7R agonist, 30 min before EA. Neurologic scoring, infarction volume, and expression of cytokines, Bcl-2 and Bax, Iba1, P2×7R, p38, and phosphorylated p38 (p-p38) in ischemia penumbra were detected 24 h after cerebral I/R.

Results

EA preconditioning ameliorated neurologic scoring, decreased infarction volume, and neuronal injury, and decreased cytokine release, while BzATP exacerbated cerebral I/R damage and inflammation events, unlike the favorable efficacy of EA. EA inhibited the expression of Iba-1, P2×7R, and p-p38/p38 in the ischemic penumbra, whereas BzATP reversed this effect.

Conclusions

EA could induce cerebral tolerance to I/R damage by suppressing P2×7R expression and release of inflammatory factors.

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电针通过调节P2×7R表达对脑缺血再灌注损伤有保护作用

背景：非化学性脑卒中是一种严重的临床疾病，难以治愈；因此，减缓ATP的消耗对于通过预处理增强缺血组织的耐受性至关重要。电针预处理诱导脑缺血耐受然而，其潜在机制尚不清楚。目的P2×7受体（P2×7R）介导小胶质细胞的刺激，参与脑缺血再灌注（I/R）损伤的发生。我们假设EA预处理的保护作用与P2×7R表达下调有关。方法以大脑中动脉闭塞模型（MCAO）为基础，建立大鼠脑I/R模型，在“百会”和“奉复”处电休克30 min。MCAO大鼠于EA前30分钟心室注射P2×7R激动剂2 '(3 ')- o -（4-苯甲酰基）三磷酸腺苷（BzATP）。脑I/R后24小时检测神经评分、梗死体积以及缺血半暗区细胞因子、Bcl-2、Bax、Iba1、P2×7R、p38和磷酸化p38 （p-p38）的表达。结果sea预处理改善了神经系统评分，减少了梗死体积，减少了神经元损伤，减少了细胞因子的释放，而BzATP则加重了脑I/R损伤和炎症事件，与EA不同，EA抑制了缺血半暗带Iba-1、P2×7R和p-p38/p38的表达，而BzATP逆转了这一作用。结论sea可通过抑制P2×7R炎症因子的表达和释放，诱导脑对I/R损伤的耐受。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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