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首页> 外文期刊>Medical Gas Research >Hydrogen inhibits microglial activation and regulates microglial phenotype in a mouse middle cerebral artery occlusion model
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Hydrogen inhibits microglial activation and regulates microglial phenotype in a mouse middle cerebral artery occlusion model

机译：氢抑制小鼠大脑中动脉闭塞模型中的小胶质细胞活化并调节小胶质细胞表型

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Microglia participate in bi-directional control of brain repair after stroke. Previous studies have demonstrated that hydrogen protects brain after ischemia/reperfusion (I/R) by inhibiting inflammation, but the specific mechanism of anti-inflammatory effect of hydrogen is poorly understood. The goal of our study is to investigate whether inhalation of high concentration hydrogen (HCH) is able to attenuate I/R-induced microglia activation. Eighty C57B/L male mice were divided into four groups: sham, I/R, I/R + HCH and I/R + Nsub2/sub/Osub2/sub groups. Assessment of animals happened in “blind” matter. I/R was induced by occlusion of middle cerebral artery for one hour). After one hour, filament was withdrawn, which induced reperfusion. Hydrogen treated I/R animals inhaled mix of 66.7% Hsub2/sub balanced with Osub2/sub for 90 minutes, starting immediately after initiation of reperfusion. Control animals (Nsub2/sub/Osub2/sub) inhaled mix in which hydrogen was replaced with Nsub2/sub for the same time (90 minutes). The brain injury, such as brain infarction and development of brain edema, as well as neurobehavioral deficits were determined 23 hours after reperfusion. Effect of HCH on microglia activation in the ischemic penumbra was investigated by immunostaining also 23 hours after reperfusion. mRNA expression of inflammation related genes was detected by PCR. Our results showed that HCH attenuated brain injury and consequently reduced neurological dysfunction after I/R. Furthermore, we demonstrated that HCH directed microglia polarization towards anti-inflammatory M2 polarization. This study indicates hydrogen may exert neuroprotective effects by inhibiting the microglial activation and regulating microglial polarization. This study was conducted in agreement with the Animal Care and Use Committee (IACUC) and Institutional Animal Care guidelines regulation (Shanghai Jiao Tong University, China (approval No. A2015-011) in November 2015.
机译：小胶质细胞参与中风后脑修复的双向控制。先前的研究表明，氢气通过抑制炎症来保护缺血/再灌注（I / R）后的大脑，但是人们对氢气的抗炎作用的具体机制了解甚少。我们研究的目的是研究吸入高浓度氢（HCH）是否能够减弱I / R诱导的小胶质细胞活化。将80只C57B / L雄性小鼠分为假手术，I / R，I / R + HCH和I / R + N 2 / O 2 四组。对动物的评估发生在“盲目”事件中。 I / R是通过大脑中动脉闭塞1小时诱导的。一小时后，抽出细丝，引起再灌注。氢气处理的I / R动物在开始再灌注后立即吸入90.7％的H 2 与O 2 平衡的混合物。对照动物（N 2 / O 2 ）吸入混合物，其中氢气同时被N 2 替代（90分钟）。在再灌注后23小时确定脑损伤，例如脑梗塞和脑水肿的发展以及神经行为缺陷。在再灌注后23小时也通过免疫染色研究了六氯环己烷对缺血性半影​​中小胶质细胞活化的影响。通过PCR检测炎症相关基因的mRNA表达。我们的结果表明，六氯环己烷可减轻脑损伤并因此减少I / R后的神经功能障碍。此外，我们证明了六氯环己烷可将小胶质细胞极化导向抗炎性M2极化。这项研究表明氢可能通过抑制小胶质细胞的活化和调节小胶质细胞的极化而发挥神经保护作用。这项研究是根据动物护理和使用委员会（IACUC）和机构动物护理指南规定（中国上海交通大学（批准号：A2015-011））于2015年11月达成的。

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