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首页> 外文期刊>Cell cycle >Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway
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Role of p75 neurotrophin receptor in neuronal autophagy in intracerebral hemorrhage in rats through the mTOR signaling pathway

机译：P75神经养素受体在大鼠脑出血中脑出血中神经营养的作用

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摘要

Rupture of weakened blood vessels could lead to severe intracerebral hemorrhage (ICH) and brain injuries. This study was designed to explore the roles of p75 neurotrophin receptor (p75(NTR)) in neuronal autophagy in ICH rats. An ICH rat model was established, and then gain and loss of functions of p75(NTR) in rat tissues were performed. Then, the pathologic morphology, water content, and inflammation in brain tissues were assessed. Western blot analysis was applied to detect the levels of inflammatory proteins, apoptosis- and autophagy-related proteins, and the mammalian target of rapamycin (mTOR) pathway-related proteins. Neuronal autophagy was further measured with mTOR activated. In vitro experiments were also performed on brain microvascular endothelial cells (BMECs) and astrocytes. Consequently, we found p75(NTR) knockdown improved the pathologic morphology with reduced neuron damage, water content, permeability of blood-brain barrier and inflammation in ICH rat brain tissues. Besides, Knockdown of p75(NTR) decreased neuronal apoptosis and inactivated mTOR signaling pathway, but it elevated the levels of autophagy-related proteins. In vivo results were reproduced in in vitro experiments. This study demonstrated that knockdown of p75(NTR) could promote neuronal autophagy and reduce neuronal apoptosis via inactivating the mTOR pathway. We hope these findings could provide new therapeutic options for ICH treatment.
机译：弱化血管破裂可能导致严重的脑内出血（ICH）和脑损伤。本研究旨在探讨P75神经养素受体（P75（NTR））在ICH大鼠神经元自噬中的作用。建立了一种ICH大鼠模型，然后进行大鼠组织中P75（NTR）的增益和失去的P75（NTR）。然后，评估病理形态，水含量和脑组织中的炎症。应用Western印迹分析来检测炎症蛋白，凋亡和自噬相关蛋白的水平，以及雷帕霉素（MTOR）途径相关蛋白的哺乳动物靶标。用MTOR活化进一步测量神经元自噬。在脑微血管内皮细胞（BMEC）和星形胶质细胞上也进行体外实验。因此，我们发现P75（NTR）敲低改善了神经元损伤，含水量，血脑屏障渗透性和ICH大鼠组织中炎症的病理形态。此外，P75（NTR）的敲低降低了神经元细胞凋亡和灭活的MTOR信号传导途径，但它升高了自噬相关蛋白质的水平。体内结果在体外实验中繁殖。本研究表明，P75（NTR）的敲低可以通过灭活MTOR途径来促进神经元自噬并降低神经元细胞凋亡。我们希望这些发现可以为ICH治疗提供新的治疗选择。

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