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Electro-acupuncture at LI11 and ST36 acupoints exerts neuroprotective effects via reactive astrocyte proliferation after ischemia and reperfusion injury in rats

机译:LI11和ST36穴位的电针对大鼠缺血和再灌注损伤后星形胶质细胞的增殖起神经保护作用

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Reactive astrogliosis is a common phenomenon in central nervous system (CNS) injuries such as ischemic stroke. The present study aimed to deeply investigate the relationships between the neuroprotective effect of electro-acupuncture (EA) and reactive astrocytes following cerebral ischemia. EA treatment at the Quchi (LI11) and Zusanli (ST36) acupoints at Day 3 attenuated neurological deficits and cerebral infarct volume in ischemia and reperfusion (I/R) injured rats. Animal behavior assessments found that the speed of Catwalk gait, equilibrium and coordination of Rotarod test were improved. Furthermore, EA treatment exerted neuroprotective effects via activation of glial fibrillary acidic protein (GFAP), vimentin and nestin positive cells. Simultaneously, an obvious increase in GFAP/vimentin, GFAPestin and GFAP/BrdU co-labeling appeared in the peri-infract cortex and striatum, suggesting EA can promote the proliferation of GFAP/vimentinestin-positive reactive astrocytes. The expression of cell cycle-associated proteins Cyclin Dl, CDK4 and phospho-Rb were increased in the peri-infract cortex and striatum, indicating proliferated reactive astrocytes-mediated CyclinDl/CDK4 regulation of the transition of the Gl-to-S cell cycle phases. In addition, EA enhanced the localized expression of brain-derived neurotrophic factor (BDNF) in the peri-infract cortex and striatum. These results demonstrated that EA treatment at the Li11 and ST36 acupoints on Day 3 exerted neuroprotection via proliferation of GFAP/vimentinestin-positive reactive astrocytes and, potentially, secretion of reactive astrocytes-derived BDNF in I/R injured rats. (C) 2015 Elsevier Inc. All rights reserved.
机译:反应性星形胶质增生是中枢神经系统(CNS)损伤(例如缺血性中风)的常见现象。本研究旨在深入研究脑缺血后电针(EA)的神经保护作用与反应性星形胶质细胞之间的关系。第3天在曲池(LI11)和祖三里(ST36)穴位进行的EA治疗减轻了缺血和再灌注(I / R)损伤大鼠的神经功能缺损和脑梗塞体积。动物行为评估发现,步态步态的速度,Rotarod试验的平衡和协调性得到了改善。此外,EA治疗通过激活胶质纤维酸性蛋白(GFAP),波形蛋白和巢蛋白阳性细胞发挥神经保护作用。同时,在周围侵犯性皮层和纹状体中出现了GFAP /波形蛋白,GFAP / nestin和GFAP / BrdU共标记的明显增加,表明EA可以促进GFAP /波形蛋白/ nestin阳性反应性星形胶质细胞的增殖。细胞周期相关蛋白Cyclin D1,CDK4和磷酸化Rb的表达在难治性周围皮层和纹状体中增加,表明增殖的反应性星形胶质细胞介导的CyclinD1 / CDK4调节了G1-S细胞周期的过渡。 。此外,EA增强了脑源性神经营养因子(BDNF)在周围性梗死皮层和纹状体中的局部表达。这些结果表明,在第3天在Li11和ST36穴位进行EA治疗可通过GFAP /波形蛋白/ nestin阳性反应性星形胶质细胞的增殖发挥神经保护作用,并可能在I / R损伤的大鼠中分泌反应性星形胶质细胞衍生的BDNF。 (C)2015 Elsevier Inc.保留所有权利。

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