丁苯酞对大鼠心肌缺血再灌注损伤的预防作用及机制研究

发布时间：2018-04-09 19:08

本文选题：丁苯酞　切入点：心肌缺血再灌注损伤　出处：《中国药房》2017年25期

【摘要】：目的:研究丁苯酞对大鼠心肌缺血再灌注损伤的预防作用及机制。方法:将SD大鼠随机分为假手术组、模型组和丁苯酞低、中、高剂量组(50、75、100 mg/kg),每组10只,各组大鼠每天ig相应药物1次,假手术组及模型组大鼠ig等量生理盐水,连续3d。末次给药后除假手术组外其余各组大鼠再灌注120 min后检测各组大鼠心肌梗死面积比例、细胞凋亡率、凋亡相关蛋白[促凋亡蛋白(Caspase-3、Fas、Caspase-9)、抑制凋亡蛋白(Bcl-2)]表达、左室射血分数(LVEF)和血清中血管内皮生长因子(VEGF)含量。结果:与假手术组比较,模型组大鼠的心肌梗死面积、心肌细胞凋亡率均明显升高,心肌细胞中Caspase-3、Fas、Caspase-9蛋白表达明显增强,Bcl-2蛋白表达明显减弱,LVEF和血清VEGF含量明显降低(P0.01)。与模型组比较,除丁苯酞低剂量组大鼠的LVEF无明显变化(P0.05)外,其余各给药组大鼠的上述指标均明显改善(P0.05)。与丁苯酞低剂量组比较,丁苯酞高剂量组大鼠的心肌梗死面积、细胞凋亡率均明显降低(P0.05);丁苯酞中、高剂量组大鼠心肌细胞中Caspase-3、Fas、Caspase-9蛋白表达明显减弱,Bcl-2蛋白表达明显增强(P0.05)。结论:丁苯酞可有效减轻大鼠心肌缺血再灌注损伤,保护心功能,其机制可能与上调VEGF有关。
[Abstract]:Aim: to study the preventive effect and mechanism of butylphthalide on myocardial ischemia reperfusion injury in rats.Methods: Sprague-Dawley rats were randomly divided into sham-operation group (n = 10), model group (n = 10) and butyphthalide low dose group (n = 10). Rats in each group were given corresponding drugs once a day. Rats in sham operation group and model group were given the same amount of saline for 3 days.After reperfusion for 120 min, the ratio of myocardial infarction size, apoptosis rate, apoptosis-related protein (Apoptosis-promoting protein Caspase-3, Fas-Fas-Caspase-9, inhibition of apoptotic protein Bcl-2) were measured.Left ventricular ejection fraction (LVEF) and serum vascular endothelial growth factor (VEGF).Results: compared with sham-operation group, myocardial infarction size and myocardial apoptosis rate in model group were significantly increased, and the expression of Caspase-3, Fas-Fas-Caspase-9 protein was significantly increased in myocardial cells. The expression of Bcl-2 protein was significantly decreased in the model group and the content of serum VEGF was significantly decreased in the model group.Compared with the model group, the above indexes in the other groups were significantly improved except for the low dose butyphthalide group (P 0.05), except for the low dose butyphthalide group (P 0.05).Compared with the low dose butyphthalide group, the myocardial infarction size and apoptosis rate of the high dose butyphthalide group were significantly lower than those of the butyphthalide group, and the expression of Caspase-3, Fas-Fas-Caspase-9 protein in the cardiomyocytes of the high-dose butyphthalide group was significantly decreased, and the expression of Bcl-2 protein was significantly enhanced.Conclusion: butyphthalide can attenuate myocardial ischemia-reperfusion injury and protect cardiac function in rats. The mechanism may be related to up-regulation of VEGF.
【作者单位】：海南省人民医院心血管内科;
【分类号】：R965

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