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首页> 外文期刊>Experimental & Molecular Pathology >Hypoxia induces microglia autophagy and neural inflammation injury in focal cerebral ischemia model
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Hypoxia induces microglia autophagy and neural inflammation injury in focal cerebral ischemia model

机译:低氧诱导局灶性脑缺血模型的小胶质细胞自噬和神经炎症损伤

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摘要

Much evidence demonstrated that autophagy played an important role in neural inflammation response after ischemia stroke. However, the specific effect of microglia autophagy in cerebral ischemia is still unknown. In the current study, we constructed focal cerebral ischemia model by permanent middle cerebral artery occlusion (pMCAO) in mice. We detected microglia autophagy and inflammation response in vivo, and observed infarct brain areas, edema formation, and neurological deficits of mice. We found that pMCAO induced microglia autophagy and inflammatory response. The suppression of autophagy using either pharmacologic inhibitor (3-MA) not only decreased the microglia autophagy and inflammatory response, but also significantly decreased infarct size, edema formation and neurological deficits in vivo. Taken together, these results suggested that cerebral ischemia induced microglia autophagy contributed to ischemic neural inflammation and injury. In addition, our findings also provided novel therapeutic strategy for ischemic stroke. (C) 2015 Elsevier Inc. All rights reserved.
机译:许多证据表明自噬在缺血性卒中后的神经炎症反应中起重要作用。然而,小胶质细胞自噬在脑缺血中的特异性作用仍然未知。在当前的研究中,我们通过永久性大脑中动脉闭塞(pMCAO)构建了小鼠局灶性脑缺血模型。我们在体内检测到小胶质细胞自噬和炎症反应,并观察了小鼠的梗塞脑区域,水肿形成和神经功能缺损。我们发现pMCAO诱导小胶质细胞自噬和炎症反应。使用任何一种药物抑制剂(3-MA)抑制自噬不仅可以减少小胶质细胞的自噬和炎症反应,而且可以显着减少体内的梗塞面积,水肿形成和神经功能缺损。综上所述,这些结果表明脑缺血引起的小胶质细胞自噬促进了缺血性神经炎症和损伤。此外,我们的发现还为缺血性中风提供了新的治疗策略。 (C)2015 Elsevier Inc.保留所有权利。

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