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缺血后处理对脑过度灌注的神经保护作用及其神经保护机制。

Neuroprotective effect of ischemic postconditioning against hyperperfusion and its mechanisms of neuroprotection.

作者信息

Bagheri Seyyed Majid, Allahtavakoli Mohammad, Hakimizadeh Elham

机构信息

Physiology-Pharmacology Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Department of Physiology and Pharmacology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

出版信息

J Res Med Sci. 2024 Jul 11;29:31. doi: 10.4103/jrms.jrms_341_22. eCollection 2024.

DOI:10.4103/jrms.jrms_341_22
PMID:39239075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11376715/
Abstract

BACKGROUND

In recent years, stroke and ischemia-reperfusion injury has motivated researchers to find new ways to reduce the complications. Although reperfusion is essential for brain survival, it is like a double-edged sword that may cause further damage to the brain. Ischemic postconditioning (IPostC) refers to the control of blood flow in postischemia-reperfusion that can reduce ischemia-reperfusion injuries.

MATERIALS AND METHODS

Articles were collected by searching for the terms: Ischemic postconditioning and neuroprotective and ischemic postconditioning and hyperperfusion. Suitable articles were collected from electronic databases, including ISI Web of Knowledge, Medline/PubMed, ScienceDirect, Embase, Scopus, Biological Abstract, Chemical Abstract, and Google Scholar.

RESULTS

New investigations show that IPostC has protection against hyperperfusion by reducing the amount of blood flow during reperfusion and thus reducing infarction volume, preventing the blood-brain barrier damage, and reducing the rate of apoptosis through the activation of innate protective systems. Numerous mechanisms have been suggested for IPostC, which include reduction of free radical production, apoptosis, inflammatory factors, and activation of endogenous protective pathways.

CONCLUSION

It seems that postconditioning can prevent damage to the brain by reducing the flow and blood pressure caused by hyperperfusion. It can protect the brain against damages such as stroke and hyperperfusion by activating various endogenous protection systems. In the present review article, we tried to evaluate both useful aspects of IPostC, neuroprotective effects, and fight against hyperperfusion.

摘要

背景

近年来,中风和缺血再灌注损伤促使研究人员寻找减少并发症的新方法。尽管再灌注对脑存活至关重要,但它就像一把双刃剑,可能会对大脑造成进一步损伤。缺血后适应(IPostC)是指在缺血再灌注后对血流的控制,可减少缺血再灌注损伤。

材料与方法

通过搜索以下术语收集文章:缺血后适应与神经保护、缺血后适应与高灌注。从电子数据库中收集合适的文章,包括ISI Web of Knowledge、Medline/PubMed、ScienceDirect、Embase、Scopus、生物学文摘、化学文摘和谷歌学术。

结果

新的研究表明,缺血后适应通过减少再灌注期间的血流量来预防高灌注,从而减少梗死体积,防止血脑屏障损伤,并通过激活先天保护系统降低细胞凋亡率。关于缺血后适应已提出了许多机制,包括减少自由基产生、细胞凋亡、炎症因子以及激活内源性保护途径。

结论

似乎后适应可以通过减少高灌注引起的血流和血压来预防脑损伤。它可以通过激活各种内源性保护系统来保护大脑免受中风和高灌注等损伤。在本综述文章中,我们试图评估缺血后适应的两个有益方面,即神经保护作用和对抗高灌注的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/233282ea933e/JRMS-29-31-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/c6d8c9937921/JRMS-29-31-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/a6ef033820e4/JRMS-29-31-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/7c0237c65f94/JRMS-29-31-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/15e1ef8d141e/JRMS-29-31-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/233282ea933e/JRMS-29-31-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/c6d8c9937921/JRMS-29-31-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/a6ef033820e4/JRMS-29-31-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/7c0237c65f94/JRMS-29-31-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/15e1ef8d141e/JRMS-29-31-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5004/11376715/233282ea933e/JRMS-29-31-g005.jpg

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本文引用的文献

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Pre- and post-conditioning with poly I:C exerts neuroprotective effect against cerebral ischemia injury in animal models: A systematic review and meta-analysis.聚肌苷酸胞苷酸预处理和后处理对动物模型脑缺血损伤发挥神经保护作用:系统评价和荟萃分析。
CNS Neurosci Ther. 2022 Aug;28(8):1168-1182. doi: 10.1111/cns.13851. Epub 2022 May 5.
3
Ischemic post-conditioning is neuroprotective even at delayed tPA administration after embolic stroke in female rats.
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Iran J Basic Med Sci. 2021 Dec;24(12):1676-1682. doi: 10.22038/IJBMS.2021.55674.12456.
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Neuroprotective effects of long noncoding RNAs involved in ischemic postconditioning after ischemic stroke.长链非编码RNA在缺血性中风后缺血后适应中的神经保护作用。
Neural Regen Res. 2022 Jun;17(6):1299-1309. doi: 10.4103/1673-5374.327346.
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The neuroprotective role of SIRT1/PGC-1α signaling in limb postconditioning in cerebral ischemia/reperfusion injury.SIRT1/PGC-1α信号通路在脑缺血/再灌注损伤肢体后处理中的神经保护作用。
Neurosci Lett. 2021 Apr 1;749:135736. doi: 10.1016/j.neulet.2021.135736. Epub 2021 Feb 15.
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Ischemic Postconditioning Reduces NMDA Receptor Currents Through the Opening of the Mitochondrial Permeability Transition Pore and K Channel in Mouse Neurons.缺血后处理通过开放线粒体通透性转换孔和 K 通道减少小鼠神经元 NMDA 受体电流。
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7
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