摘要
目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂triglitazone对血管紧张素Ⅱ(AngⅡ)刺激内皮细胞分泌血管活性因子的影响。方法以脐静脉内皮细胞为研究对象,观察triglitazone对内皮细胞分泌血管活性因子内皮素-1(ET-1)和一氧化氮(NO)的影响。结果10μmol/L和50μmol/L的triglitazone使人脐静脉内皮细胞分泌ET-1含量与对照组相比虽有下降但无统计学意义,而NO与对照组相比明显升高(P<0.05);50μmol/L triglitazone可明显抑制AngⅡ(1×10-6mol/L)所刺激的ET的分泌(P<0.05);两种浓度triglitazone均能抑制AngⅡ对内皮细胞生成NO的减低作用(P<0.05)。结论Triglitazone可抑制AngⅡ所刺激的内皮细胞合成和分泌ET-1的增加和NO的减少,提示triglitazone可通过影响血管活性因子的产生而参与血压的调节。
Objective To investigate the effect of PPAR γ ligand triglitazone on the secretion of ET-1 and NO from endothelial cells stimulated by Ang Ⅱ. Methods The cultured human umbilical vein endothelial cells （HUVECs） were treated with Ang Ⅱ and triglitazone. Chemiluminescence analysis was used to measure the concentration of NO, and radioimmunoassay method was used to detect the production of ET-1. Results The HUVECs were treated with 10 μmol/L and 50 μmol/L triglitazone. The concentration of ET-1 in cell culture supernatants decreased without statistical significance. The concentration of NO increased significantly compared with that of the control （P〈0. 05）. 50μmol/L triglitazone inhibited the production of Ang Ⅱ （1 × 10^-6 mol/L） - induced ET-1 obviously （P〈0. 05）, and both 10μmol/L and 50μmol/L triglitazone could inhibit the effect of Ang Ⅱ, which decreased NO release from the endothelial cells, indicating that the concentration of NO increased obviously （P〈0. 05）. Conclusion Triglitazone can inhibit the effect of Ang Ⅱ on endothelial cells, which enhances the production of ET-1 but decreases the synthesis and release of NO, showing that triglitazone has relation with the modulation of blood pressure.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2006年第6期538-540,581,共4页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
陕西省科技攻关基金资助项目(No.2004K14-G1)
