异丙酚抑制高糖诱导的脐静脉内皮细胞黏附分子表达

 目的  研究异丙酚抑制高糖诱导的脐静脉内皮细胞黏附分子的表达并探讨其可能的机制。方法  采用Histopaque-1077溶液提取人外周血单核细胞。采用一氧化氮(NO)试剂盒检测脐静脉内皮细胞NO生成。采用Western blot检测内皮细胞黏附分子、内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)(总蛋白,单体及双体)、eNOS磷酸化水平及caveolin-1表达。结果  高糖上调血管内皮细胞黏附分子1(vascular cell adhesion molecule,VCAM-1)的表达,促进单核细胞-内皮黏附,并减少NO生成。异丙酚改善高糖环境下NO生成,并抑制VCAM-1表达及单核细胞-内皮黏附。异丙酚的作用可被eNOS抑制剂L-NAME所拮抗。异丙酚能上调高糖环境下eNOS-Ser1177磷酸化水平及双体/单体比值,下调高糖环境下eNOS-Thr495磷酸化水平及caveolin-1表达。结论  异丙酚通过调节高糖环境下eNOS的磷酸化水平、单体/双体比值及caveolin-1表达,改善内皮细胞NO生成,进而抑制内皮细胞黏附分子的表达及单核细胞-内皮细胞的黏附。

Propofol inhibits high glucose induced expression of endothelial adhesion molecule in umbilical vein endothelial cells

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-Ser1177phosphrylation 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.