异丙酚抑制高糖诱导的脐静脉内皮细胞黏附分子表达.

Objective To study high glucose induced expressiont of endothelial adhesion molecule inhibited by propofol in umbilical vein endothelial cells, and to investigate its mechanism. Methods Human peripheral mononuclear cells were prepared with Histopaque-1077 solution. Nitric oxide (NO) production was measured with an assay kit. Vascular cell adhesion molecule 1 (VCAM-1) expression, endothelial nitric oxide synthase (eNOS) total protein, dimer and monomer expression, eNOS phosphorylation and caveolin-1 were measured by Western blot. Results High glucose induced VCAM-1 expression, increased mononuclear-endothelial adhesion and reduced NO production. Propofol improved NO level, and inhibited VCAM-1 expression and mononuclear-endothelial adhesion. The protective effect of propofol would be blocked by an eNOS inhibitor of L-NAME. Propofol increased high glucose-mediated eNOS-Ser1177 phosphrylation and dimmer/monomer ratio, and attenuated high glucose-induced eNOS-Thr495 phosphrylation and caveolin-1 expression. Conclusions Propofol improved high glucose mediated eNOS phosphrylation, dimer/monomer ratio and caveolin-1 expression, so that NO production was improved and VCAM-1 expression and mononuclear-endothelial interaction were inhibited. [ABSTRACT FROM AUTHOR]