二甲双胍减轻软脂酸诱导的血管内皮细胞损伤机制探讨

程莹; 母义明; 汪保安; 潘长玉; 陆菊明

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二甲双胍减轻软脂酸诱导的血管内皮细胞损伤机制探讨

论著 | 更新时间：2026-01-09

- 二甲双胍减轻软脂酸诱导的血管内皮细胞损伤机制探讨
- Protective mechanism of metformin in process of human umbilical vein endothelial cell injury induced by palmitic acid in vitro
- 陆军军医大学学报 2008年30卷第14期页码：1357-1359
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  中图分类号： R322.12;R589.2;R966
- 纸质出版：2008
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程莹,母义明,汪保安,潘长玉,陆菊明.二甲双胍减轻软脂酸诱导的血管内皮细胞损伤机制探讨[J].陆军军医大学学报(原第三军医大学学报),2008,30(14):1357-1359.

　CHENG Ying,MU Yi-ming,WANG Bao-an,PAN Chang-yu,LU Ju-ming.Protective mechanism of metformin in process of human umbilical vein endothelial cell injury induced by palmitic acid in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(14):1357-1359.
程莹,母义明,汪保安,潘长玉,陆菊明.二甲双胍减轻软脂酸诱导的血管内皮细胞损伤机制探讨[J].陆军军医大学学报(原第三军医大学学报),2008,30(14):1357-1359. DOI：

　CHENG Ying,MU Yi-ming,WANG Bao-an,PAN Chang-yu,LU Ju-ming.Protective mechanism of metformin in process of human umbilical vein endothelial cell injury induced by palmitic acid in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(14):1357-1359. DOI：

摘要

目的了解二甲双胍在软脂酸（PA）诱导的血管内皮细胞损伤中的保护作用及机制。方法人脐静脉血管内皮细胞（HUVEC）在空白对照、PA、二甲双胍和PA联合二甲双胍培养液中培养24 h。RT-PCR方法测定单核细胞趋化蛋白-1（MCP-1）和细胞间黏附分子-1（ICAM-1）的mRNA表达，Western blot测定24 h细胞的ICAM-1、核因子κB p65（NF-κB p65）和磷酸化抑制因子κBα（IκBα）的蛋白表达。结果与对照组相比，PA组的MCP-1和ICAM-1表达显著增加（P0.05）。加入二甲双胍后，MCP-1和ICAM-1表达显著减少（P0.05）。二甲双胍降低PA诱导的NF-κB p65和磷酸化IκBα表达增加。结论二甲双胍可能通过激活AMPK，阻断PA对NF-κB的激活，减少MCP-1和ICAM-1表达，从而减轻PA诱导的HUVEC损伤。

Abstract

Objective To explore the protective mechanism of metformin in the process of cultured human umbilical vein endothelial cells (HUVECs) injury induced by palmitic acid (PA). Methods HUVECs were cultured in the media of blank

metformin

or PA combined metformin for 24 h

48 h

72 h respectively. Expressions of monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) were determined by RT-PCR and the expressions of ICAM-1

nuclear factor kappa B p65 (NF-κB p65) and phospho-IκBα was evaluated by Western blotting. Results Significant increase of the expressions of MCP-1 and ICAM-1 was found in PA group compared with in the control group (P0.05). However

obvious decrease was observed in both group when metformin was added (P0.05). The increase of the expressions of NF-κB p65 and phospho-IκBα induced by PA was also abated by metformin. Conclusion Metformin can alliviate the HUVECs injury induced by PA by activating AMPK

reducing the expression of MCP-1 and ICAM-1 activated by NF-κB.

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