蛋白激酶C在脑缺血再灌注损伤中的作用

摘要/Abstract

摘要： 缺血性脑卒中以其高发病率、高致残率和高死亡率严重危害着人类健康。缺血性脑损伤的病理生理机制极为复杂,其涉及到许多相关基因和蛋白(如:凋亡易感基因、Bcl-2蛋白家族、谷胱甘肽过氧化物酶及热休克蛋白等)的表达变化。目前FDA认证的治疗缺血性脑卒中的药物仅有重组组织型纤溶酶原激活剂(Recombinant tissue plasminogen activator, rtPA)一种。其主要原因是缺血性脑损伤是由如炎症、自由基等多种因素导致的,而多数药物仅作用于个别或少数靶点,且副作用明显,导致治疗结果不佳,因此对新型药物的研究和开发成了治疗缺血性脑卒中的重点。研究发现蛋白激酶C(Protein kinase C, PKC)可能参与调节脑缺血再灌注损伤,并有望成为治疗缺血性脑卒中的新靶点。本文就PKC及各个亚型在缺血再灌注损伤中的作用作一系统综述。

关键词: 缺血性脑卒中, 蛋白激酶C, 机制, 炎症, 自由基

Abstract: Ischemic stroke is seriously hurting human health because of its high morbidity, disability rate and mortality. The pathophysiology mechanism is very complicated, which involves in expression exchanges of many genes and proteins (sensitive to apoptosis gene, Bcl-2 family proteins, glutathione perodxidase and heat shock protein). Only recombinant tissue plasminogen activator (rtPA) is currently being used in treatment of ischemic stroke by FDA. For multi-factors as inflammation and free radicals, contribute to ischemic stroke, however, many drugs, with few targets and significant side effects, cause a suboptimal therapeutic outcome. So developing new drugs in treatment of ischemic stroke will be an important issue. Some data demonstrated that PKC is likely to involve in mediating ischemic brain injury and may be a promising therapeutic target. Here the role of PKC and PKC isozymes in ischemic reperfusion injury will be discussed.

Key words: Ischemic stroke, PKC, Mechanism, Inflammation, Free radicals

中图分类号:

R743.3

张凤云, 赵炎, 吴玉林. 蛋白激酶C在脑缺血再灌注损伤中的作用[J]. 中国临床药理学与治疗学, 2013, 18(4): 461-468.

ZHANG Feng-yun, ZHAO Yan, WU Yu-lin. Effect of protein kinase C on cerebral ischemic reperfusion injury[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2013, 18(4): 461-468.

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