Electroacupuncture reduces corpus callosum injury in rats with permanent cerebral ischemia by inhibiting the activation of high-mobility group box 1 protein and the receptor for advanced glycation end products.

IF 1.6 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2024-10-16 Epub Date: 2024-07-30 DOI:10.1097/WNR.0000000000002084

Chenyu Li, Zeyin Nie, Huachun Miao, Feng Wu, Xiuxiu Wang

{"title":"Electroacupuncture reduces corpus callosum injury in rats with permanent cerebral ischemia by inhibiting the activation of high-mobility group box 1 protein and the receptor for advanced glycation end products.","authors":"Chenyu Li, Zeyin Nie, Huachun Miao, Feng Wu, Xiuxiu Wang","doi":"10.1097/WNR.0000000000002084","DOIUrl":null,"url":null,"abstract":"<p><p>Previous studies have shown that cerebral ischemia can cause white matter injury in the brain. This study aimed to investigate the potential mechanism of electroacupuncture (EA) at the Baihui (GV20) and Zusanli (ST36) acupoints in protecting white matter. Sprague-Dawley rats were used to establish permanent middle cerebral artery occlusion (pMCAO) rat models. Comprehensive motor functions were assessed using the mesh experiment. Morphological changes in the myelin sheath were assessed with Luxol fast blue staining. Morphological changes in oligodendrocytes and myelinated axons were evaluated using Nissl staining. The expressions of high-mobility group box 1 protein (HMGB1) and the receptor for advanced glycation end products (RAGE) in the corpus callosum were detected by immunohistochemical staining and Western blot analysis. pMCAO caused severe injury to the corpus callosum, evidenced by significant loss of white matter fibers and myelinated axons, and induced overexpression of HMGB1 and RAGE in the corpus callosum. EA treatment significantly improved comprehensive motor function alleviated white matter damage, and downregulated the expression of HMGB1 and RAGE. Its effects were comparable to those of FPS-ZM1, a RAGE receptor inhibitor. In conclusion, EA effectively improves comprehensive motor function in rats with cerebral infarction and alleviates corpus callosum injury. This effect may be related to the inhibition of HMGB1 and RAGE overexpression.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"963-971"},"PeriodicalIF":1.6000,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11389880/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroreport","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/WNR.0000000000002084","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/30 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Previous studies have shown that cerebral ischemia can cause white matter injury in the brain. This study aimed to investigate the potential mechanism of electroacupuncture (EA) at the Baihui (GV20) and Zusanli (ST36) acupoints in protecting white matter. Sprague-Dawley rats were used to establish permanent middle cerebral artery occlusion (pMCAO) rat models. Comprehensive motor functions were assessed using the mesh experiment. Morphological changes in the myelin sheath were assessed with Luxol fast blue staining. Morphological changes in oligodendrocytes and myelinated axons were evaluated using Nissl staining. The expressions of high-mobility group box 1 protein (HMGB1) and the receptor for advanced glycation end products (RAGE) in the corpus callosum were detected by immunohistochemical staining and Western blot analysis. pMCAO caused severe injury to the corpus callosum, evidenced by significant loss of white matter fibers and myelinated axons, and induced overexpression of HMGB1 and RAGE in the corpus callosum. EA treatment significantly improved comprehensive motor function alleviated white matter damage, and downregulated the expression of HMGB1 and RAGE. Its effects were comparable to those of FPS-ZM1, a RAGE receptor inhibitor. In conclusion, EA effectively improves comprehensive motor function in rats with cerebral infarction and alleviates corpus callosum injury. This effect may be related to the inhibition of HMGB1 and RAGE overexpression.

查看原文本刊更多论文

电针通过抑制高移动组盒 1 蛋白和高级糖化终产物受体的活化，减轻永久性脑缺血大鼠胼胝体的损伤。

以往的研究表明，脑缺血可导致脑白质损伤。本研究旨在探讨电针百会穴（GV20）和足三里穴（ST36）保护脑白质的潜在机制。研究使用 Sprague-Dawley 大鼠建立永久性大脑中动脉闭塞（pMCAO）大鼠模型。通过网状实验对大鼠的综合运动功能进行评估。髓鞘的形态学变化采用鲁索快蓝染色法进行评估。用 Nissl 染色法评估少突胶质细胞和有髓鞘轴突的形态变化。免疫组化染色和 Western 印迹分析检测了胼胝体中高迁移率组盒 1 蛋白（HMGB1）和高级糖化终产物受体（RAGE）的表达。 pMCAO 对胼胝体造成了严重损伤，表现为白质纤维和有髓鞘轴突的显著缺失，并诱导胼胝体中 HMGB1 和 RAGE 的过度表达。EA治疗可明显改善综合运动功能，减轻白质损伤，并下调HMGB1和RAGE的表达。其效果与RAGE受体抑制剂FPS-ZM1相当。总之，EA能有效改善脑梗死大鼠的综合运动功能，减轻胼胝体损伤。这种作用可能与抑制 HMGB1 和 RAGE 过度表达有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

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.