川芎嗪对氧化型低密度脂蛋白诱导的血管内皮细胞损伤的保护作用

Protective effect of ligustrazine on oxidized LDL-induced injury of vascular endothelial cells

目的探讨川芎嗪对氧化型低密度脂蛋白(ox-LDL)诱导的血管内皮细胞损伤的保护作用及其分子机制。方法体外培养人冠状动脉内皮细胞,并随机分为对照组、ox-LDL组、不同浓度川芎嗪为1μmol/L组、10μmol/L组、100μmol/L组。用RT-PCR及Western blot法检测单核细胞趋化蛋白1(MCP-1)和细胞间黏附分子1(ICAM-1)基因和蛋白表达;采用免疫荧光法观察NF-κB p65蛋白的核转位。结果与对照组比较,ox-LDL组MCP-1、ICAM-1基因和蛋白表达明显升高(P<0.01);与ox-LDL组比较,10μmol/L组、100μmol/L组MCP-1、ICAM-1基因表达明显降低(P<0.01),1μmol/L组、10μmol/L组MCP-1、ICAM-1蛋白表达明显降低(P<0.01)。免疫荧光显示,1μmol/L组、10μmol/L组可抑制NF-κB p65亚基的核转位。结论川芎嗪对ox-LDL诱导的血管内皮细胞损伤有保护作用。

Objective To study the protective effect of ligustrazine （LIG） on oxidized LDL （ox-LDL）-induced injury of vascular endothelial cells and its mechanism. Methods In vitro cul- tured human coronary artery endothelial cells were randomly divided into control group, ox-LDL group,1 μmol/L LIG group, 10 μmol/L LIG group,and 100 μmol/L LIG group. Expression of monocyte chemoattraetant protein 1 （MCP-1） and intercellular adhesion molecule 1 （ICAM-1） mRNA was detected by RT-PCR and Western blot, respectively. Nuclear translocation of NF-κB p65 protein was observed with immunofluorescent staining. Results The expression level of MCP-1 and ICAM-1 was significantly higher in ox-LDL group than in control group（P〈0.01） and significantly lower in 10μmol/L and 100μmol/L LIG groups than in control group（P〈0.01） Immunofluorescence showed that the nuclear transloeation of NF-κB p65 protein was inhibited in 1μmol/L and 10 μmol/L LIG groups（P〈0. 01）. Conclusion LIG can protect vascular endothelial cells against ox-LDL-induced injury.