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Preface high hyperhomocysteinemia ( HHcy ) is an independent risk factor for atherosclerosis ( AS ) . But its advice to the AS specific molecular mechanism is not very clear. At present, most studies suggest that high Hcy causes vascular endothelial dysfunction, is part of the initiating AS . Therefore, in-depth study HHcy mechanism of injury on endothelial cell function is particularly important. Is well known that vascular endothelial cells can synthesize and secrete vascular relaxing factor NO shrinkage factor ET. Under normal circumstances, both to maintain balance and stability , to maintain the state of the contraction and relaxation of the blood vessels . When the endothelial cell damage , the generation of NO and release defects balance in favor of ET, leading to vasoconstriction in vivo Movement advantages diastolic dysfunction . Vasodilation is reduced , the is AS earliest performance . Studies have shown that under physiological conditions , NO is produced by endothelial cells by eNOS - specific catalytic L - arginine to generate ; vascular ET system endothelial cells produce ET-1 expression . Another experiment showed that Hcy can lead to endothelial cells secrete ET-1 was significantly higher increase in ET - 1 mRNA expression ; generate NO decreased , of eNOSmRNA decreased expression . Suggesting that HHcy impact vascular endothelial cells eNOSmRNA and the ET -1 mRNA expression . In this study, the culture of HUVEC ECV304 cells subjected to different concentrations of Hcy detection of eNOS and E T - 1 transcription level , in order to prove that the damage of Hcy on endothelial function , and then explore the mechanism of its advice to the AS . Materials and experimental methods , experimental materials , experimental cells : human umbilical vein endothelial cells ECV304 cell lines , reagents and drugs : homocysteine, fetal bovine serum , RPMI1640 medium , Trizol RNA extraction reagent , RT -PCR kit , eNOS primers , ET-1 primer beta - actin primers , PBS buffer , penicillin and streptomycin .
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