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miR-137 prevents inflammatory response oxidative stress neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

机译:miR-137通过阻断Src介导的MAPK信号转导通路在缺血性卒中中预防炎症反应氧化应激神经元损伤和认知障碍

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摘要

Stroke is a leading cause of death and disability worldwide. The purpose of this study was to investigate the possible role of the microRNA (miRNA or miR) miR-137 in ischemic stroke. miRNAs are very stable in the blood and may serve as potential diagnostic and therapeutic markers. Wild-type, and miR-137 mice were treated with siRNA or siRNA to identify their roles in the inflammatory response, oxidative stress, neuronal injury and cognitive impairment in brain tissues of mice following middle cerebral artery occlusion (MCAO) operation. We evaluated several factors including; inflammatory responses, oxidative stress, viability and apoptosis of astrocytes in order to identify the functions of miR-137 and in ischemic stroke. miR-137 alleviated the inflammatory response, oxidative stress, neuronal injury and cognitive impairment, and restricted apoptosis via targeting and inactivating the MAPK signaling pathway. Furthermore, up-regulation of miR-137 or inhibition of inhibited the secretion of inflammatory factors, suppressed oxidative stress, and reduced apoptosis of astrocytes. In conclusion, our work suggests that, in mice, miR-137 confers neuroprotective effects against ischemic stroke via attenuation of oxidative, apoptotic, and inflammatory pathways through inhibiting -dependent MAPK signaling pathway.
机译:中风是导致全球死亡和残疾的主要原因。这项研究的目的是调查microRNA(miRNA或miR)miR-137在缺血性中风中的可能作用。 miRNA在血液中非常稳定,可以用作潜在的诊断和治疗标记。用siRNA或siRNA处理野生型和miR-137小鼠,以鉴定它们在大脑中动脉闭塞(MCAO)手术后小鼠脑组织的炎症反应,氧化应激,神经元损伤和认知障碍中的作用。我们评估了以下几个因素:星形胶质细胞的炎症反应,氧化应激,活力和凋亡,以鉴定miR-137和缺血性中风的功能。 miR-137通过靶向和失活MAPK信号通路来减轻炎症反应,氧化应激,神经元损伤和认知障碍,并限制细胞凋亡。此外,miR-137的上调或抑制可抑制炎症因子的分泌,抑制氧化应激并减少星形胶质细胞的凋亡。总之,我们的工作表明,在小鼠中,miR-137通过抑制依赖的MAPK信号传导途径减弱氧化,凋亡和炎症途径,从而赋予了针对缺血性中风的神经保护作用。

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