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New progress of isoflurane, sevoflurane and propofol in hypoxic‐ischemic brain injury and related molecular mechanisms based on p 75 neurotrophic factor receptor
Author(s) -
Zhu Yi,
Zhou HongSu,
Chen DongQin,
Zhou Di,
Zhao Nan,
Xiong LiuLin,
Deng Issac,
Zhou XinFu,
Zhu ZhaoQiong
Publication year - 2021
Publication title -
ibrain
Language(s) - English
Resource type - Journals
eISSN - 2769-2795
pISSN - 2313-1934
DOI - 10.1002/j.2769-2795.2021.tb00075.x
Subject(s) - isoflurane , neuroprotection , propofol , neurotrophic factors , sevoflurane , neurotrophin , neuroscience , medicine , mechanism (biology) , anesthesia , calpain , brain derived neurotrophic factor , pharmacology , receptor , bioinformatics , biology , philosophy , biochemistry , enzyme , epistemology
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 p 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.

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