Suppr超能文献

缺血后处理和远隔预处理的神经保护作用。临床应用前景

[Neuroprotective effect of ischemic postconditioning and remote preconditioning. Prospective of clinical use].

作者信息

Maslov L N, Lishmanov Iu B

出版信息

Angiol Sosud Khir. 2012;18(2):27-34.

Abstract

Ischemic postconditioning enhances brain and spinal cord tolerance to ischemia and reperfusion. There are no clinical data on the neuroprotective effect of postconditioning. It was established that foregoing effect of ischemic postconditioning depended upon an activation of PKCs, ERK, Akt kinases and a decrease in the activity of JNK kinase. Superoxide dismutase, Bax, Bal-2 and HSP proteins may be the end effector of postconditioning. Postconditioning phenomenon is mimicked by norepinephrine, diazoxide, sevoflurane, isoflurane and propofol. It is unknown before whether these pharmacological agents prevent brain reperfusion injury in human. Remote preconditioning improves brain and spinal cord tolerance to ischemic and reperfusion damages. There are no data on the neuroprotective effect of remote preconditioning in human at ischemic insult. The endogenous cannabinoids, reactive oxygen species are triggers of remote preconditioning. The neuroprotective effect of preconditioning at distance is depended on the activation of p38, ERK kinases and is attributed to enhancement of HSP-70 protein synthesis.

摘要

缺血后处理可增强脑和脊髓对缺血及再灌注的耐受性。目前尚无关于后处理神经保护作用的临床数据。已证实缺血后处理的上述作用依赖于蛋白激酶C(PKCs)、细胞外信号调节激酶(ERK)、蛋白激酶B(Akt)激酶的激活以及应激活化蛋白激酶(JNK)激酶活性的降低。超氧化物歧化酶、Bax、Bcl-2和热休克蛋白(HSP)可能是后处理的终效应分子。去甲肾上腺素、二氮嗪、七氟醚、异氟醚和丙泊酚可模拟后处理现象。此前尚不清楚这些药物是否能预防人类脑再灌注损伤。远程预处理可提高脑和脊髓对缺血及再灌注损伤的耐受性。目前尚无关于人类在缺血性损伤时远程预处理神经保护作用的数据。内源性大麻素、活性氧是远程预处理的触发因素。远程预处理的神经保护作用依赖于p38、ERK激酶的激活,并归因于热休克蛋白70(HSP-70)合成的增强。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验