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目的:探讨奥美沙坦酯对急性心肌梗死(AMI)大鼠骨髓内皮祖细胞(endothelial progenitor cells,EPCs)动员的影响。方法:结扎SD大鼠左冠状动脉前降支制作AMI模型,将术后24 h存活的24只大鼠随机分为3组:AMI组、奥美沙坦酯1 mg·kg-1·d-1组(OML组)和奥美沙坦酯3 mg·kg-1·d-1组(OMH组);另设假手术组(8只)作为对照。灌胃给药共2周。大鼠尾动脉血压计测量大鼠收缩压,ELISA法测定血清血管内皮生长因子(VEGF)含量,以DiI标记的乙酰化低密度脂蛋白(DiI-acLDL)及FITC标记的单叶豆凝集素1(FITC-BS-1)双色荧光标记鉴定循环及骨髓EPCs并对其计数。结果:在术前,术后24 h、1周及2周各组大鼠尾动脉收缩压之间差异无统计学意义;与假手术组比较,AMI组、OML组和OMH组的血清VEGF含量、循环和骨髓EPCs数量均明显升高;与AMI组比较,OML组和OMH组血清VEGF含量无明显变化,循环和骨髓EPCs数量却明显增加。结论:大鼠AMI后2周骨髓EPCs的动员增加,奥美沙坦酯能显著促进AMI大鼠骨髓EPCs的动员,增加循环EPCs数量,此效应与VEGF途径及血压降低无明显相关。
Objective: To investigate the effects of olmesartan medoxomil on the mobilization of bone marrow endothelial progenitor cells (EPCs) in acute myocardial infarction (AMI) rats. Methods: AMI model was established by ligating left anterior descending coronary artery of SD rats. 24 rats survived 24 h after operation were randomly divided into 3 groups: AMI group, olmesartan medoxomil 1 mg · kg -1 · d -1 (OML group) and olmesartan (3 mg · kg -1 · d -1) group (OMH group), and sham-operated group (8) as control group. Gavage for a total of 2 weeks. The rat systolic blood pressure was measured by rat tail arterial sphygmomanometer. The content of serum vascular endothelial growth factor (VEGF) was measured by ELISA. DiI-acLDL and FITC-labeled single bean lectin 1 (FITC-BS-1) dual-color fluorescent labeling of circulating and bone marrow EPCs and counting. Results: There was no significant difference in the systolic pressure of the caudal artery between the two groups at 24 h, 1 week and 2 weeks after operation. Compared with sham operation group, serum VEGF level in AMI group, OML group and OMH group , And the number of circulating EPCs and bone marrow EPCs were significantly increased. Compared with AMI group, serum VEGF levels in OML group and OMH group did not change significantly, and the number of circulating and bone marrow EPCs increased significantly. CONCLUSION: Mobilization of EPCs in bone marrow of AMI rats increased 2 weeks after AMI. Olmesartan medoxomil could significantly promote the mobilization of EPCs in bone marrow of AMI rats and increase the number of circulating EPCs. This effect was not significantly associated with VEGF pathway and blood pressure reduction.