Endothelial dysfunction and Protein kinase C activity development interrelation at ischemic injury of a brain.

A V Voronkov, A V Mamleev
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Abstract

The ischemic stroke is the reason of high mortality and population disability worldwide and it is closely connected with endothelium dysfunction (ED). The endothelium carries out regulation of specific functions, generally the universal modulator - nitrogen oxide. A number of enzymes participates in a production of nitric oxide, but specific for an endothelium is endothelial NO synthase (eNOS), which violation of regulation is observed at an ischemic stroke. Significant role in activity of eNOS regulation plays protein kinase C (PKC). In this review the following processes were investigated: ED and nitric oxide interrelation at an ischemic stroke; some features of biological activity of nitric oxide depending on a place of synthesis and on time of ischemic damage; eNOS activity regulation by means of PKC; interrelation between ED and PKC activity at oxidative stress; the main alarm ways including activation of eNOS and PKC which regulate microvascular permeability and a tone of vessels of a brain. Being guided by the carried-out analysis of theoretical data, it should be noted that at development of ED the PKC hyperactivity is observed, therefore, the search of the substances possessing inhibiting influence on activity of PKC for treatment of the majority of cardiovascular diseases and an ischemic stroke has become particularly important and perspective.

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缺血性脑损伤中内皮功能障碍与蛋白激酶C活性发展的相互关系。
缺血性脑卒中是世界范围内死亡率和致残率较高的疾病之一,与内皮细胞功能障碍(ED)密切相关。内皮细胞进行特定功能的调节,一般是通用调节剂——氮氧化物。许多酶参与一氧化氮的产生,但内皮细胞特异性的是内皮NO合成酶(eNOS),在缺血性中风中观察到其违反调节。蛋白激酶C (PKC)在eNOS活性调控中起重要作用。在这篇综述中,研究了以下过程:ED和一氧化氮在缺血性卒中中的相互关系;一氧化氮生物活性随合成地点和缺血损伤时间的变化特征PKC对eNOS活性的调控氧化应激下ED与PKC活性的相互关系;主要的报警方式包括eNOS和PKC的激活,它们调节微血管的通透性和大脑血管的张力。在已开展的理论数据分析的指导下,应该注意到,在ED的发展过程中观察到PKC的过度活跃,因此,寻找对PKC活性有抑制作用的物质来治疗大多数心血管疾病和缺血性中风变得尤为重要和有前景。
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