Electroacupuncture ameliorating post-stroke cognitive impairments via inhibition of peri-infarct astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia.
Electroacupuncture ameliorating post-stroke cognitive impairments via inhibition of peri-infarct astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia.
复制标题
电针通过抑制梗塞周围星形胶质细胞和小胶质细胞/巨噬细胞 P2 嘌呤受体介导的神经炎症和增生来改善中风后认知障碍
DOI：
10.1186/s12906-017-1974-y
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发表时间：
2017-10-10
影响因子：
--
通讯作者：
Chen L
中科院分区：
文献类型：
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作者：
Huang J;You X;Liu W;Song C;Lin X;Zhang X;Tao J;Chen L
缺血性卒中（IS）时，梗死核心区受损神经细胞释放ATP，激活梗死周围神经胶质细胞P2嘌呤受体，引起促炎细胞因子分泌，可能引发或加重运动和认知功能障碍。电针是一种安全有效的抗炎治疗方法。但电针对中枢神经系统嘌呤受体的作用尚未见报道。采用大脑中动脉闭塞再灌注（MCAO/R）法建立大鼠脑缺血再灌注损伤模型。电针组大鼠于MCAO/R损伤后12 h开始，连续7 d电针DU 20、DU 24穴位。观察缺血后大鼠的神经功能、梗死体积、梗死灶周围海马CA 1区和感觉运动区星形胶质细胞和小胶质细胞/巨噬细胞增生、炎性细胞因子、P2 X7 R和P2 Y1 R表达的变化，评价电针治疗MCAO/R的作用机制。与MCAO/R模型和非EA治疗相比，EA有效地降低了促炎细胞因子白细胞介素-1 β（IL-1β）的水平，如通过减少星形胶质细胞和小胶质细胞/巨噬细胞增生以及梗死周围海马CA 1和感觉运动皮层中P2 X7 R和ED 1、P2 X7 R和GFAP、P2 Y1 R和ED 1、P2 Y1 R和GFAP共表达的水平所证明的，伴随着改善的神经缺陷和运动和记忆障碍的结果。因此，我们的数据支持的假设，EA可以发挥其抗炎作用，通过抑制星形胶质细胞和小胶质细胞/巨噬细胞P2嘌呤受体（P2 X7 R和P2 Y1 R）介导的神经炎症后MCAO/R损伤。缺血性中风后电针治疗可减轻梗死周围海马CA 1区和感觉运动皮层中星形胶质细胞和小胶质细胞/巨噬细胞P2嘌呤受体介导的神经炎症和增生，并伴有运动和记忆行为表现的改善。本文的在线版本（10.1186/s12906-017-1974-y）包含补充材料，可供授权用户使用。
During ischemic stroke (IS), adenosine 5′-triphosphate (ATP) is released from damaged nerve cells of the infract core region to the extracellular space, invoking peri-infarct glial cellular P2 purinoceptors singling, and causing pro-inflammatory cytokine secretion, which is likely to initiate or aggravate motor and cognitive impairment. It has been proved that electroacupuncture (EA) is an effective and safe strategy used in anti-inflammation. However, EA for the role of purine receptors in the central nervous system has not yet been reported. Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. The neurological outcomes, infarction volumes and the level of astroglial and microglial/macrophage hyperplasia, inflammatory cytokine and P2X7R and P2Y1R expression in the peri-infarct hippocampal CA1and sensorimotor cortex were investigated after IS to evaluate the MCAO/R model and therapeutic mechanism of EA treatment. EA effectively reduced the level of pro-inflammatory cytokine interleukin-1β (IL-1β) as evidenced by reduction in astroglial and microglial/macrophage hyperplasia and the levels of P2X7R and ED1, P2X7R and GFAP, P2Y1R and ED1, P2Y1R and GFAP co-expression in peri-infarct hippocampal CA1 and sensorimotor cortex compared with that of MCAO/R model and Non-EA treatment, accompanied by the improved neurological deficit and the motor and memory impairment outcomes. Therefore, our data support the hypothesis that EA could exert its anti-inflammatory effect via inhibiting the astroglial and microglial/macrophage P2 purinoceptors (P2X7R and P2Y1R)-mediated neuroinflammation after MCAO/R injury. Astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia in peri-infarct hippocampal CA1 and sensorimotor cortex were attenuated by EA treatment after ischemic stroke accompanied by the improved motor and memory behavior performance. The online version of this article (10.1186/s12906-017-1974-y) contains supplementary material, which is available to authorized users.