罗格列酮抑制高糖诱导的内皮细胞黏附作用
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Rosiglitazone Inhibits Glucose-Induced Adherent Effects on Human Umbilical Vein Endothelial Cells
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    目的研究罗格列酮对高糖诱导的内皮细胞黏附作用的影响。方法应用不同浓度葡萄糖处理内皮细胞后,加入不同浓度罗格列酮,用免疫细胞化学法和逆转录聚合酶链反应分别检测血管细胞黏附分子1蛋白及mRNA的表达。同时各处理组行内皮细胞-单核细胞黏附试验。结果葡萄糖可诱导血管细胞黏附分子蛋白和mRNA的表达明显增加(P<0.05),在16.7mmol/L时作用最显著;应用罗格列酮后,血管细胞黏附分子1蛋白和mRNA的表达明显降低(P<0.05)。葡萄糖可诱导内皮细胞-单核细胞黏附增加,且与葡萄糖浓度呈正相关;罗格列酮可抑制内皮细胞-单核细胞黏附(P<0.05)。结论在一定葡萄糖浓度范围内,罗格列酮可能通过抑制葡萄糖诱导的内皮细胞血管细胞黏附分子1的表达来抑制内皮细胞-单核细胞的黏附作用,这可能是罗格列酮抗糖尿病相关的动脉粥样硬化作用之一。

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    Aim To investigate the effect of rosiglitazone(RSG) on glucose-induced adhesion of human endothelial cells.Methods Endothelial cells were incubated with different concentrations of glucose,and then treated with different concentrations of rosiglitazone.Vascular cell adhesion molecule-1(VCAM-1) protein and mRNA expression was detected by immunocytochemical method and RT-PCR.Endothelial-monocyte adhesion assays were carried out in treated cells.Results VCAM-1 mRNA and protein expression were increased significantly with glucose concentration increased,which was obvious at 16.7 mmol/L glucose group(P<0.05).Compared with RSG untreated group,relative VCAM-1 mRNA and protein expression decreased to varying degrees in the RSG treated group(P<0.05).Furthermore,endothelial-monocyte adhesion increased with increment of glucose concentration(P<0.05) and decreased after treatment of high dose RSG(P<0.05).Conclusions RSG may appear to have direct anti-diabetes-associated-atherosclerosis which is at least partly due to effects on VCAM-1 expression induced by glucose,which leads to decreased endothelial-monocyte adhesion and macrophage infiltration.

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彭扬,王玉霞,李慧,孟馨.罗格列酮抑制高糖诱导的内皮细胞黏附作用[J].中国动脉硬化杂志,2009,17(3):185~188.

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  • 收稿日期:2009-01-07
  • 最后修改日期:2009-03-02
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