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

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.