Electroacupuncture reduces oxidative stress response and improves secondary injury of intracerebral hemorrhage in rats by activating the peroxisome proliferator-activated receptor-γ/nuclear factor erythroid2-related factor 2/γ-glutamylcysteine synthetase pathway.

IF 1.6 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2024-04-08 DOI:10.1097/wnr.0000000000002026

Weigang Luo, Wei Bu, Hequn Chen, Wanhu Liu, Xudong Lu, Guisong Zhang, Cuicui Liu, Xiaohui Li, Huiling Ren

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引用次数: 0

Abstract

Intracerebral hemorrhage (ICH) is a severe stroke subtype. Secondary injury is a key factor leading to neurological deficits after ICH. Electroacupuncture (EA) can improve the neurological function after ICH, however, its internal mechanism is still unclear. The aim of this study is to investigate whether EA could ameliorate secondary injury after ICH through antioxidative stress and its potential regulatory mechanism. A rat model of ICH was established by injecting autologous blood into striatum. After the intervention of EA and EA combined with peroxisome proliferator-activated receptor-γ (PPARγ) blocker, Zea-longa scores, modified neurological severity scores and open field tests were used to evaluate the neurological function of the rats. Flow cytometry detected tissue reactive oxygen species (ROS) levels. Tissue tumor necrosis factor-α (TNF-α) levels were analyzed by enzyme-linked immunosorbent assays. The protein expressions of PPAR γ, nuclear factor erythroid2-related factor 2 (Nrf2) and γ-glutamylcysteine synthetase (γ-GCS) were detected by Western blot. Immunohistochemistry was used to observe the activation of microglia. The demyelination degree of axon myelin was observed by transmission electron microscope. Compared with the model group, EA intervention improved neurological function, decreased ROS and TNF-α levels, increased the protein expression of PPARγ, Nrf2 and γ-GCS, and reduced the activation of microglia, it also alleviated axonal myelin sheath damage. In addition, the neuroprotective effect of EA was partially attenuated by PPARγ blocker. EA ameliorated the neurological function of secondary injury after ICH in rats, possibly by activating the PPARγ/Nrf2/γ-GCS signaling pathway, reducing microglia activation, and inhibiting oxidative stress, thus alleviating the extent of axonal demyelination plays a role.

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电针通过激活过氧化物酶体增殖物激活受体-γ/核因子红细胞2相关因子2/γ-谷氨酰半胱氨酸合成酶途径，降低氧化应激反应，改善大鼠脑出血继发性损伤。

脑出血（ICH）是一种严重的中风亚型。继发性损伤是导致 ICH 后神经功能缺损的关键因素。电针（EA）可以改善 ICH 后的神经功能，但其内在机制尚不清楚。本研究旨在探讨电针能否通过抗氧化应激改善 ICH 后的继发性损伤及其潜在的调节机制。通过向大鼠纹状体注射自体血，建立了大鼠 ICH 模型。EA和EA联合过氧化物酶体增殖激活受体-γ（PPARγ）阻断剂干预后，Zea-longa评分、改良神经系统严重程度评分和野外开放试验用于评估大鼠的神经功能。流式细胞术检测组织活性氧（ROS）水平。组织肿瘤坏死因子-α（TNF-α）水平通过酶联免疫吸附试验进行分析。用 Western 印迹法检测 PPAR γ、核因子红细胞相关因子 2（Nrf2）和γ-谷氨酰半胱氨酸合成酶（γ-GCS）的蛋白表达。免疫组化用于观察小胶质细胞的活化。透射电子显微镜观察轴突髓鞘的脱髓鞘程度。与模型组相比，EA干预改善了神经功能，降低了ROS和TNF-α水平，增加了PPARγ、Nrf2和γ-GCS的蛋白表达，降低了小胶质细胞的活化，还减轻了轴突髓鞘的损伤。此外，PPARγ阻断剂可部分减弱EA的神经保护作用。EA能改善大鼠ICH后继发性损伤的神经功能，可能是通过激活PPARγ/Nrf2/γ-GCS信号通路、减少小胶质细胞活化和抑制氧化应激，从而减轻轴突脱髓鞘的程度发挥了作用。

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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来源期刊

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.