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疾病阶段相关的学习和记忆改变通过电针对阿尔茨海默病小鼠皮层小胶质细胞 M1/M2 极化的调节。

Disease Stage-Associated Alterations in Learning and Memory through the Electroacupuncture Modulation of the Cortical Microglial M1/M2 Polarization in Mice with Alzheimer's Disease.

机构信息

College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.

Fujian Key Laboratory of Rehabilitation Technology, Fuzhou, Fujian 350122, China.

出版信息

Neural Plast. 2020 Aug 28;2020:8836173. doi: 10.1155/2020/8836173. eCollection 2020.

Abstract

Microglia are the primary cells that exert immune function in the central nervous system, and accumulating evidence suggests that microglia act as critical players in the initiation of neurodegenerative disorders, such as Alzheimer's disease (AD). Microglia seemingly demonstrate two contradictory phenotypes in response to different microenvironmental cues, the M1 phenotype and the M2 phenotype, which are detrimental and beneficial to pathogenesis, respectively. Inhibiting the M1 phenotype with simultaneous promoting the M2 phenotype has been suggested as a potential therapeutic approach for cure AD. In this study, we demonstrated that electroacupuncture at the Shenting and Baihui acupoints for 16 weeks could improve learning and memory in the Morris water maze test and reduce amyloid -protein in the parietal association cortex and entorhinal cortex in mice with mild and moderate AD. Besides, electroacupuncture at the Shenting and Baihui acupoints not only suppressed M1 marker (iNOS/IL-1) expression but also increased the M2 marker (CD206/Arg1) expression in those regions. We propose that electroacupuncture at the Shenting and Baihui acupoints could regulate microglial polarization and decrease A plaques to improve learning and memory in mild AD mice.

摘要

小胶质细胞是中枢神经系统中发挥免疫功能的主要细胞,越来越多的证据表明,小胶质细胞在神经退行性疾病(如阿尔茨海默病)的发病机制中起着关键作用。小胶质细胞对不同的微环境信号表现出两种相反的表型,即 M1 表型和 M2 表型,它们分别对发病机制有有害和有益的影响。抑制 M1 表型并同时促进 M2 表型已被提议作为治疗阿尔茨海默病的潜在治疗方法。在这项研究中,我们证明了对轻度和中度 AD 小鼠进行 16 周的神庭和百会穴电针治疗可以改善其在 Morris 水迷宫测试中的学习和记忆能力,并减少顶叶联合皮层和内嗅皮层中的淀粉样蛋白。此外,神庭和百会穴电针不仅抑制了这些区域的 M1 标志物(iNOS/IL-1)表达,还增加了 M2 标志物(CD206/Arg1)的表达。我们提出,神庭和百会穴电针可能通过调节小胶质细胞极化和减少 A 斑块来改善轻度 AD 小鼠的学习和记忆能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b5/7474773/c1dcf4fecc5d/NP2020-8836173.001.jpg

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