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基于75种神经营养因子受体的异氟烷、七氟烷和丙泊酚在缺氧缺血性脑损伤中的新进展及相关分子机制

New progress of isoflurane, sevoflurane and propofol in hypoxic-ischemic brain injury and related molecular mechanisms based on 75 neurotrophic factor receptor.

作者信息

Zhu Yi, Zhou Hong-Su, Chen Dong-Qin, Zhou Di, Zhao Nan, Xiong Liu-Lin, Deng Issac, Zhou Xin-Fu, Zhu Zhao-Qiong

机构信息

School of Anesthesiology Zunyi Medical University Zunyi Guizhou China.

Department of Anesthesia Hospital of Stomatology, Zunyi Medical University Zunyi Guizhou China.

出版信息

Ibrain. 2021 Jun 28;7(2):132-140. doi: 10.1002/j.2769-2795.2021.tb00075.x. eCollection 2021 Jun.

Abstract

Hypoxic ischemic brain injury (HIBI) is one of the most common clinical disorders, especially in neonates. The complex pathophysiology of HIBI is an important cause of disability and even death of patients, however, being without effective clinical treatments. Common anesthetics (such as isoflurane, propofol and sevoflurane) have an adverse impact on neuronal cells for HIBI via the regulation of 75 neurotrophic factor receptor (P75NTR). In order to protect the injured brains and study the effect of underlying treatments, it is particularly significant to understand and master the developmental mechanism of anesthetics for the occurrence of HIBI related molecular mechanisms. Therefore, this paper will mainly review the corresponding pathogenic and protective mechanisms about HIBI binding to the research progress of the role of P75NTR. In conclusion, the effects of neuroprotection and injured nerves are involved in the expression and activation of P75NTR, mainly increased P75NTR mRNA, protein levels and calpain-dependent for propofol, and inducing neuronal apoptosis for isoflurane and sevoflurane, and we look forward to that connection with P75NTR, common anaesthetic and HIBI may be a new direction of research and gain perfect outcomes in the future.

摘要

缺氧缺血性脑损伤(HIBI)是最常见的临床病症之一,尤其是在新生儿中。HIBI复杂的病理生理学是导致患者残疾甚至死亡的重要原因,然而目前尚无有效的临床治疗方法。常见的麻醉剂(如异氟烷、丙泊酚和七氟烷)通过调节75神经营养因子受体(P75NTR)对HIBI患者的神经元细胞产生不利影响。为了保护受损大脑并研究潜在治疗方法的效果,了解和掌握麻醉剂对HIBI发生相关分子机制的发展机制尤为重要。因此,本文将主要结合P75NTR作用的研究进展,综述HIBI相应的致病和保护机制。总之,神经保护和神经损伤的作用涉及P75NTR的表达和激活,主要表现为丙泊酚使P75NTR mRNA、蛋白水平升高且依赖钙蛋白酶,而异氟烷和七氟烷则诱导神经元凋亡,我们期待与P75NTR相关的研究、常见麻醉剂和HIBI可能成为未来一个新的研究方向并取得理想成果。

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Cell Mol Neurobiol. 2022 May;42(4):1153-1166. doi: 10.1007/s10571-020-01006-x. Epub 2020 Nov 17.
3
Neural stem cell therapies and hypoxic-ischemic brain injury.神经干细胞治疗与缺氧缺血性脑损伤。
Prog Neurobiol. 2019 Feb;173:1-17. doi: 10.1016/j.pneurobio.2018.05.004. Epub 2018 May 21.

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