电针通过刺激PPAR-γ调节氧化应激、神经元死亡和神经炎症,减轻脑缺血再灌注损伤。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
ACS Applied Bio Materials Pub Date : 2024-06-01 Epub Date: 2024-02-13 DOI:10.1177/09645284231211600
Nanfang Cheng, Xinyuan Cheng, Feng Tan, Yangui Liang, Lihong Xu, Jian Wang, Jiuqing Tan
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引用次数: 0

摘要

背景:氧化应激和炎症反应在脑缺血再灌注(I/R)损伤中起着至关重要的作用。电针(EA)在中国被广泛用作脑卒中的康复治疗方法,但其潜在的作用机制仍不清楚。据报道,过氧化物酶体增殖激活受体γ(PPAR-γ)具有抗炎和抗氧化作用:本研究探讨了 PPAR-γ 在 EA 介导的效应中的作用,并旨在阐明其在脑 I/R 中的可能机制:本研究以雄性Sprague-Dawley(SD)大脑中动脉闭塞/再灌注(MCAO/R)损伤大鼠为研究对象,在MCAO/R后连续7天每天用LI11和ST36浓度的EA治疗30 min。通过神经行为评估、三苯基氯化四氮唑染色、苏木精-伊红染色和透射电子显微镜检测了EA的神经保护作用。通过酶联免疫吸附试验、免疫荧光和逆转录酶聚合酶链反应检测氧化应激、炎症因子、神经凋亡和小胶质细胞活化。用 Western 印迹法评估 PPAR-γ 介导的信号传导:结果:我们发现 EA 能明显减轻 I/R 引发的脑梗死体积,降低神经系统评分,抑制 I/R 引发的氧化应激、炎症反应和小胶质细胞活化。EA 还能增加 PPAR-γ 蛋白的表达。此外,注射 PPAR-γ 拮抗剂 T0070907 会逆转 EA 的保护作用:结论:EA通过刺激PPAR-γ调节氧化应激、神经元死亡和神经炎症,从而减轻脑I/R损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electroacupuncture attenuates cerebral ischemia/reperfusion injury by regulating oxidative stress, neuronal death and neuroinflammation via stimulation of PPAR-γ.

Background: Oxidative stress and inflammatory responses play essential roles in cerebral ischemia/reperfusion (I/R) injury. Electroacupuncture (EA) is widely used as a rehabilitation method for stroke in China; however, the underlying mechanism of action remains unclear. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has been reported to impact anti-inflammatory and anti-oxidative effects.

Objective: This study investigated the role of PPAR-γ in EA-mediated effects and aimed to illuminate its possible mechanisms in cerebral I/R.

Methods: In this study, male Sprague-Dawley (SD) rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury were treated with EA at LI11 and ST36 for 30 min daily after MCAO/R for seven consecutive days. The neuroprotective effects of EA were measured by neurobehavioral evaluation, triphenyltetrazolium chloride staining, hematoxylin-eosin staining and transmission electron microscopy. Oxidative stress, inflammatory factors, neural apoptosis and microglial activation were examined by enzyme-linked immunosorbent assay, immunofluorescence and reverse transcriptase polymerase chain reaction. Western blotting was used to assess PPAR-γ-mediated signaling.

Results: We found that EA significantly alleviated cerebral I/R-induced infarct volume, decreased neurological scores and inhibited I/R-induced oxidative stress, inflammatory responses and microglial activation. EA also increased PPAR-γ protein expression. Furthermore, the protective effects of EA were reversed by injection of the PPAR-γ antagonist T0070907.

Conclusion: EA attenuates cerebral I/R injury by regulating oxidative stress, neuronal death and neuroinflammation via stimulation of PPAR-γ.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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