NO NOS and ischemia-reperfusion injury in Progress.doc

 PAGE \* MERGEFORMAT 13 NO NOS and ischemia-reperfusion injury in Progress Keywords:: nitric oxide; nitric oxide synthase; ischemia-reperfusion injury Summary of nitric oxide and nitric oxide synthase in ischemia-reperfusion injury has important implications, but the experimental results are the opposite conclusion, which is observed in all experimental animal species, experimental conditions, different from the phase point in time. The need for further research. Keywords: nitric oxide; nitric oxide synthase; ischemia-reperfusion injury In recent years, nitric oxide (NO) and nitric oxide synthase (NOS) on the effects of ischemia-reperfusion injury caused widespread concern, this article in ischemia-reperfusion in the process of research to make an overview of the status quo. Dependent on the NOS, NO biosynthesis NOS classification, distribution and regulation of NOS is divided into two categories, namely, the native-type NOS (constitutive nOS, cNOS) and inducible NOS (inducible NOS, iNOS). To its molecular level, studies have shown that endothelial cells and neurons derived from the expression of gene sequences generated are not the same, but its activity are dependent on calcium and calmodulin, it in turn divided into neurogenic NOS (ncNOS) and endothelial cell NOS (ecNOS0). the biological activity of iNOS is not dependent on calcium and calmodulin, in general did not express. Be a number of cytokines such as interleukin-1β (IL-1β ), tumor necrosis factor-α (TNFα )-induced activation. Although all three NOS genes that encode different, but the structural similarity, and therefore there are also similarity function [1]. In addition to three kinds of NOS are mainly distributed in the cytoplasm of the soluble components, but also exists in a number of sub-cellular devices in [2], different organizations may have the same kind of NOS, but in the same organization the same kinds of NOS, in different states may be their function is different. Recently f