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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
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| 篇名： | 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 |
| TITLE： | |
| 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3 d。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（P＜0.01）。与模型组比较，除丁苯酞低剂量组大鼠的LVEF无明显变化（P＞0.05）外，其余各给药组大鼠的上述指标均明显改善（P＜0.05）。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（P＜0.05）；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（P＜0.05）。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： | OBJECTIVE： To study the preventive effect and mechanism of butylphthalide on myocardial ischemia-reperfusion injury in rats. METHODS： SD rats were randomly divided into sham operation group， model group， butylphthalide low-dose， medium-dose， high-dose groups （50， 75， 100 mg/lg）， 10 in each group. All rats were intragastrically administrated related drugs once a day， sham operation group and model group were intragastrically administrated equal amount of normal saline， for 3 d. After last administration， except for sham operation group， 120 min of repertusion was conducted. Ratio of myocardial infarction area， apoptosis rate of myocardial cells， expressions of apoptosis-related protein [proapoptotic proteins （Caspase-3， Fas， Caspase-9）， apoptotic protein （Bcl-2）]， left ventricular ejection fraction （LVEF）， and content of vascular endothelial growth factor （VEGF） in serum of rats in other groups were detected. RESULTS： Compared with sham operation group， myocardial infarction area and apoptosis rate of myocardial cells in model group were obviously increased； expressions of Caspase-3， Fas， Caspase-9 protein in myocardial cells were obviously enhanced， Bcl-2 protein expression was obviously weakened； LVEF and serum VEGF content were obviously reduced （P＜0.01）. Compared with model group， except that LVEF in butylphthalide low-dose group didn’t changed obviously （P＞0.05）， above indexes in other administration groups improved obviously （P＜0.05）. Compared with butylphthalide low-dose group， myocardial infarction area and apoptosis rate of myocardial cells in butylphthalide high-dose group were obviously decreased （P＜0.05）； expressions of Caspase-3， Fas， Caspase-9 protein in myocardial cells in butylphthalide medium-dose， high-dose groups were obviously weakened， and Bcl-2 protein expression was obviously enhanced （P＜0.05）. CONCLUSIONS： Butylphthalide can effectively reduce myocardial ischemia-reperfusion injury in rats， protect cardiac functions， and its mechanism may be related with up-regulating VEGF. |
| 期刊： | 2017年第28卷第25期 |
| 作者： | 周菲，张敬文，王卫 |
| AUTHORS： | ZHOU Fei，ZHANG Jingwen，WANG Wei |
| 关键字： | 丁苯酞；心肌缺血再灌注损伤；细胞凋亡；大鼠 |
| KEYWORDS： | Butylphthalide； Myocardial ischemia-reperfusion injury； Cell apoptosis； Rats |
| 阅读数： | 408 次 |
| 本月下载数： | 4 次 |
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