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Inhibition of mammalian target of rapamycin improves neurobehavioral deficit and modulates immune response after intracerebral hemorrhage in rat

机译:抑制雷帕霉素的哺乳动物靶点可改善大鼠脑出血后的神经行为缺陷并调节免疫反应

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摘要

BackgroundMammalian target of rapamycin (mTOR), a serine/threonine kinase, regulates many processes, including cell growth and the immune response. mTOR is also dysregulated in several neurological diseases, such as traumatic brain injury (TBI), stroke, and neurodegenerative disease. However, the role of mTOR in intracerebral hemorrhage (ICH) remains unexplored. The aims of our study were to determine whether inhibiting mTOR signaling could affect the outcome after ICH and to investigate the possible underlying mechanism.
机译:背景雷帕霉素(mTOR)的哺乳动物靶标是一种丝氨酸/苏氨酸激酶,可调节许多过程,包括细胞生长和免疫反应。 mTOR在几种神经系统疾病中也失调,例如脑外伤(TBI),中风和神经退行性疾病。但是,mTOR在脑出血(ICH)中的作用尚待探索。我们研究的目的是确定抑制mTOR信号传导是否会影响ICH后的预后并研究可能的潜在机制。

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