前列腺素E1对人脐静脉内皮细胞单核细胞趋化蛋白-1表达的影响  

Effect of prostaglandin E1 on the expression of MCP-1 in cultured human umbilical vein endothelial cells

作　　者：李方雄[1] 卢桂静[1] 周胜华[2] 沈向前[2] 祁述善[2] 

机构地区：[1]中南大学湘雅医院心内科,长沙市410008 [2]中南大学湘雅二医院

出　　处：《中华老年医学杂志》2008年第5期355-357,共3页Chinese Journal of Geriatrics

摘　　要：目的探讨前列腺素E1（PGE1）对人脐静脉内皮细胞单核细胞趋化蛋白-1（monocyte chemoattactant protein-1，MCP-1）表达的影响及可能机制。方法用培养的人脐静脉内皮细胞观察氧化低密度脂蛋白（ox-LDL）对MCP-1、核因子（NF）-κB表达的影响及PGE，的干预作用。采用ELISA检测上清液MCP-1浓度，原位杂交检测MCP-1 mRNA的表达，免疫印迹检测NF—κB蛋白表达。结果（1）PGE1（0.001、0．010、0．100mol／L）组与ox-LDL（100μg/ml）组比较，MCP-1蛋白表达为（0．327±0．051）、（0．214±0．213）、（0．247±0．228）pg／ml对（0．655±0．013）pg／ml，MCP-1 mRNA表达为（0．061±0．008）、（0.033±0．006）、（0．026±0．004）吸光度（A）／μm^2对（0．220±0．032）μm^2，PGE1显著抑制了ox-LDL所诱导的MCP-1改变。（2）Western blot结果显示，PGE1呈浓度依赖性抑制ox-LDL所诱导的NF-κBP65蛋白表达。结论PGE1可抑制ox—LDI，诱导的内皮细胞MCP—1及NF-κB表达上调，这可能与PGE1介导的血管内皮保护作用有关。Objective To investigate the effect of prostaglandin EI（PGE1） on the expression of monocyte chemoattractant protein-1 （MCP-1）in human umbilical vein endothelial cells （HUVECs） and its possible mechanism. Methods Endothelial cells were incubated with oxidized low-density lipoprotein （ox-LDL group） in the presence or absence of prostaglandin El. The level of MCP-1 in the supernatants was determined by enzyme linked immunosorbent assay （ELISA）, the expression of MCP-1 mRNA in cultured endothelial cells was detected by in-situ hybridization and the protein expression of NF-κB was analyzed by Western blot. Results Compared with ox-LDL（100μg/ml）, PGE1 markedly lowered the levels of MCP-1[（0. 327±0. 051）,（0. 214±0. 213）, （0. 247 ±0. 228）pg/ ml vs. （0. 655±0. 013）pg/ml], inhibiting the expression of MCP-1 mRNA [（0. 061±0. 008）, （0. 033 ±0.006）,（0.026±0.004）A/μm^2 vs. （0.220±0. 032）A/μm^2] in the cultured HUVECs in a dose-dependent manner （0. 001, 0.01, 0.1 mol/L）. Western blot analysis demonstrated that the amount of NF-κB p65 was attenuated after treatment with prostaglandin E1 for 24 hours. Conclusions Prostaglandin E1 can downregulate the expressions of MCP-1 and NF-κB induced by ox-LDL in HUVECs, which may thereby defend the blood vessel endothelial cell function.

关 键 词：前列地尔 趋化因子CCL2 脐静脉 内皮细胞 NF—κB 

分 类 号：R686[医药卫生—骨科学]