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作 者:刘晓琴 段文婷 李佳薇 汤沁涵 陶晨煜 张池玉 LIU Xiaoqin;DUAN Wenting;LI Jiawei;TANG Qinhan;TAO Chenyu;ZHANG Chiyu(School of Medicine,Shanxi Datong University,Datong Shanxi,037009)
出 处:《山西大同大学学报(自然科学版)》2024年第6期80-84,共5页Journal of Shanxi Datong University(Natural Science Edition)
基 金:山西省应用基础研究计划项目[20210302124276];山西大同大学大学生创新创业训练计划项目[XDC2022194];山西大同大学基础青年科研基金项目[2022Q21]。
摘 要:阿尔茨海默病(Alzheimer’s disease,AD)的发生发展与小胶质细胞(Microglia,MG)调节的神经炎性反应密切相关。当脑内稳态被破坏时,MG被激活。MG有两种激活态:M1型和M2型。M1型分泌促炎因子,导致神经毒性;M2型分泌抗炎因子,发挥抗炎及损伤修复作用。促进MG从M1型向M2型转化被认为是一种有效治疗AD的途径。ROCK2是一种丝氨酸/苏氨酸激酶,在AD病人及AD动物模型脑内被异常激活,下调ROCK2活性能够促进AD小鼠脑内MG从M1型向M2型转化,显著降低AD小鼠的神经炎性反应。对近年来下调ROCK2活性调控MG极化来防治AD的作用机制予以综述。Microglia(MG)regulated neuroinflammatory response plays critical roles on the pathogenesis of Alzheimer’s disease(AD).When brain homeostasis is disrupted,MG is activated.MG has two phenotypes:M1 phenotype and M2 phenotype.M1-like MG secretes pro-inflammatory factors,leading to neurotoxicity;M2-like MG secretes anti-inflammatory factors and plays the role of anti-inflammatory and damage repair.Promoting the conversion of MG from M1 phenotype to M2 phenotype is considered as an effective way for AD therapy.ROCK2,a serine/threonine kinase,is abnormally activated in the brains of AD patients and AD animal models.Previous studies have proved that inhibition of ROCK2 activity can promote the conversion of MG from M1 to M2 phenotype in the brains of AD mice,and significantly attenuates the neuroinflammation of AD mice.The present article focuses on recent findings regarding the down regulation of ROCK2 activity in regulation MG polarization to prevent AD.
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