氨氯地平对糖基化低密度脂蛋白诱导的血管内皮功能障碍的修复作用

Role of amlodipine action to restore the vascular endothelial dysfunction induced by glycated low density lipoproteins

目的研究氨氯地平(Am)对糖基化低密度脂蛋白(AGE-LDL)诱导的内皮功能障碍的修复作用。方法以AGE-LDL于体外模拟糖尿病合并脂代谢异常环境,将人脐静脉内皮细胞(HEC,来自EA.hy926细胞系)分别在AGE-LDL及AGE-LDL+Am环境中孵育,并以天然LDL(nLDL)孵育组为对照,应用实时PCR检测细胞中单核细胞趋化蛋白-1(MCP-1)、血管细胞粘附分子-1(VCAM-1)的基因表达水平变化,应用WesternBlot检测培养液中MCP-1蛋白量的变化。结果与nLDL组细胞相比,AGE-LDL组细胞中MCP-1、VCAM-1基因表达水平明显升高,培养液中MCP-1蛋白含量亦明显增多;在AGE-LDL中加入Am处理后,与AGE-LDL组细胞相比,细胞中MCP-1、VCAM-1基因表达水平明显下降,培养液中MCP-1蛋白含量亦明显减少。结论氨氯地平在糖尿病合并动脉粥样硬化所致内皮细胞功能障碍方面具有修复及保护作用。

Objective To study the role of amlodipine action to restore the vascular endothelial dysfunction in duced by glycated low density lipoproteins （AGELDL）. Methods Human endothelial cells （ HEC, from EA. hy926 line） were incubated with native LDL and AGELDL in the presence/absence of Am, and the gene expression of MCP 1 and VCAM1 were determined by real time PCR, the protein of MCP1 in the culture medium were determined by Western Blot. Results Combined with nLDL,AGELDL induced an increase of the mRNA of MCP1 and VCAM1, and improved the secretion of the protein of MCP1 more significantly ;Am induced a down regulation of the gene ex pression of MCP1 and VCAM1 and decreased the MCP1 protein secretion compared with AGELDL. Conclusion Amlodipine plays a role of restoring and protecting the endothelial dysfunction in diabetes complicated with atheroscle rosis.