PPARγ对ECV-304细胞ICAM-1与VCAM-1表达的影响

Effect of PPARγ on the expression of ICAM-1 and VCAM-1 in ECV-304 cells

目的观察过氧化物酶体增殖物激活型受体γ(PPARγ)对糖基化终末产物(AGEs)所诱导的血管内皮细胞表达ICAM-1、VCAM-1的影响,探讨PPARγ在糖尿病血管并发症及动脉粥样硬化中的可能作用。方法体外培养人内皮细胞系ECV-304,应用PPARγ的反义寡核苷酸及激动剂处理细胞,采用流式细胞仪及Western印迹技术检测细胞中ICAM-1及VCAM-1蛋白质的表达。结果反义阻断PPARγ在mRNA水平上的表达,ECV-304细胞ICAM-1及VCAM-1的表达上调,而PPARγ激动剂Ciglitizone则降低ICAM-1及VCAM-1的表达。结论PPARγ激活可负调控AGEs诱导的血管内皮细胞ICAM-1和VCAM-1的表达,这是PPARγ抑制糖尿病血管并发症及动脉粥样硬化发生发展的可能机制之一。

Objective In order to observe the effect of peroxisome proliferator-activated receptor gamma （PPARγ） on the expression of intercellular adhesion molecule-1 （ICAM-1） and vascular cell adhesion molecule-1 （VCAM-1） induced by glycation end products （AGEs） in human ECV-304 cell line. To investigate the role of PPARγ in the pathogenesis of diabetic vascular disease and athemsclerosis. Methods Human ECV- 304 cell were cultured in RPMI-1640 supplemented with 10% FCS. Antisense strategy and Ciglitizone were used to investigate the role of PPARγ in the endothelial cells. The expression of ICAM-1 and VCAM-1 was detected by flow cytometry and western blotting. Results The expression of ICAM-1 and VCAM-1 were upregulated by PPARγ antisense oligonucleotides, and were downregulated by Ciglitizone in ECV-304 cells in a concentration-dependent manner. Condusion pPARγ may play a negative regulation of the expression of ICAM-1 and VCAM-1 induced by AGEs in ECV-304 cells. This may be a mechanism that PPARγ inhibites diabetic vascular disease and atherosclemsis.