Suppr超能文献

电针对永久性大脑缺血大鼠胼胝体损伤的作用机制:抑制高迁移率族蛋白 B1 及晚期糖基化终产物受体的激活。

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.

机构信息

Department of Human Anatomy, Wannan Medical College, Wuhu, Anhui, China.

出版信息

Neuroreport. 2024 Oct 16;35(15):963-971. doi: 10.1097/WNR.0000000000002084. Epub 2024 Jul 30.

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.

摘要

先前的研究表明,脑缺血可导致大脑白质损伤。本研究旨在探讨电针对百会(GV20)和足三里(ST36)穴位保护白质的潜在机制。使用 Sprague-Dawley 大鼠建立永久性大脑中动脉闭塞(pMCAO)大鼠模型。采用网格实验评估综合运动功能。采用卢索快速蓝染色评估髓鞘的形态变化。用尼氏染色评估少突胶质细胞和髓鞘轴突的形态变化。用免疫组织化学染色和 Western blot 分析检测胼胝体中高迁移率族蛋白 B1(HMGB1)和晚期糖基化终产物受体(RAGE)的表达。pMCAO 导致胼胝体严重损伤,表现为白质纤维和髓鞘轴突明显丢失,并诱导胼胝体中 HMGB1 和 RAGE 的过度表达。电针治疗可显著改善综合运动功能,减轻白质损伤,并下调 HMGB1 和 RAGE 的表达。其作用与 RAGE 受体抑制剂 FPS-ZM1 相当。总之,电针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 的过度表达有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/520e/11389880/b8ed5c7b44c4/nr-35-0963-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验