Effect of Exendin-4 on nitric oxide release from pig iliac endothelial cells

刘浩宇; 胡小春; 张冬颖; 覃数

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Effect of Exendin-4 on nitric oxide release from pig iliac endothelial cells

更新时间：2026-01-09

- Effect of Exendin-4 on nitric oxide release from pig iliac endothelial cells
- Journal of Army Medical University Vol. 34, Issue 14, Pages: 1430-1433(2012)
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  CLC： R322.121;R329.26;R977.15
- Published：2012
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刘浩宇,胡小春,张冬颖,覃数.Exendin-4对猪髋动脉内皮细胞NO释放的影响[J].陆军军医大学学报(原第三军医大学学报),2012,34(14):1430-1433.

　Liu Haoyu,Hu Xiaochun,Zhang Dongying,Qin Shu.Effect of Exendin-4 on nitric oxide release from pig iliac endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(14):1430-1433.
刘浩宇,胡小春,张冬颖,覃数.Exendin-4对猪髋动脉内皮细胞NO释放的影响[J].陆军军医大学学报(原第三军医大学学报),2012,34(14):1430-1433. DOI：

　Liu Haoyu,Hu Xiaochun,Zhang Dongying,Qin Shu.Effect of Exendin-4 on nitric oxide release from pig iliac endothelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(14):1430-1433. DOI：

摘要

目的观察Exendin-4（Ex-4）对猪髋动脉内皮细胞（pig iliac endothelium cell lines，PIEC）释放一氧化氮（NO）的影响，及其与细胞内外钙浓度的关系。方法免疫荧光法检测确认PIEC上存在胰高血糖素样肽-1受体（glucagon-like peptide-1，GLP-1R）；Griess重氮化反应检测Ex-4对有钙、无钙2种培养基条件下内皮细胞NO释放的影响，流式细胞仪检测细胞内钙浓度，评价Ex-4诱导PIEC释放NO的时效-量效关系。给予内皮型一氧化氮合成酶（eNOS）信号阻断剂左旋-硝基精氨酸甲脂（L-NAME）预处理后，观察Ex-4对PIEC释放NO的影响。结果 PIEC上有GLP-1受体表达。Ex-4能刺激PIEC释放NO，作用有剂量及时间依赖关系，同时细胞内钙离子浓度也有升高[（62.67±1.53）vs（57.36±1.42），P0.01]。无钙培养液组PIEC释放NO较有钙培养液组升高更明显[（2.014±1.040）μmol/L vs （1.624±0.424）μmol/L，P=0.03]。Ex-4刺激PIEC释放NO L-NAME预处理后，Ex-4诱导的PIEC释放NO减少（P0.01）。结论 Ex-4通过激活eNOS增加内皮细胞NO释放，其eNOS激活作用可能与细胞内外钙离子变化相关。

Abstract

Objective To observe the effect of Exendin-4（Ex-4）on nitric oxide (NO）release from pig iliac endothelial cells (PIEC) and its relation with intra- and extracellular calcium concentrations. Methods Glucagon-like peptide-1 receptor (GLP-1R) was detected in PIEC with immunofluorescence assay. Effect of Ex-4 on NO release from PIEC was detected by Griess diazonium reaction in medium with calcium or without calcium. Intracellular calcium concentration was measured with a flow cytometer. Relation between time and concentration effectiveness of Ex-4-induced NO release from PIEC was assessed. Effect of Ex-4 on NO release from PIEC was observed after pretreated with the eNOS signal blocker

L-NAME. Results The GLP-1R was expressed in PIEC. Ex-4 stimulated the NO release from PIEC in a dose- and time-dependent manner. The intracellular calcium concentration was higher than the extracellular calcium concentration (62.67±1.53 vs 57.36±1.42，P0.01）. The NO release level was significantly higher from PIEC in the medium without calcium than in the medium with calcium (2.014±1.040 vs 1.624±0.424 μmol/L

P=0.03）. The Ex-4-induced NO release from PIEC after pretreatment than before pretreatment with L-NAME（P0.01）. Conclusion Ex-4 increases NO release from PIEC by activating eNOS. The role of Ex-4 in activating eNOS may be related with the intracellular calcium concentration.

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