摘要
目的:观察灯盏花素(breviscapine,bre)对大鼠心肌缺血再灌注损伤诱导的细胞凋亡的影响并探讨其机制。方法:采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注模型。40只SD大鼠随机分为正常对照组(control)、缺血再灌注组(ischemiareperfusion,IR)和灯盏花素组。灯盏花素组大鼠于术前1周分别腹腔注射不同剂量的灯盏花素(25、50 mg.kg-1.d-1),另2组给予等量生理盐水。缺血30min、再灌注2h后,采用TUNEL法检测心肌细胞凋亡情况,western blotting检测Caspase-3蛋白表达的变化。结果:缺血再灌注组凋亡指数和Caspase-3蛋白表达较正常对照组明显升高(P<0.01),灯盏花素组各指标较缺血再灌注组降低(P<0.05,P<0.01)。结论:灯盏花素对大鼠心肌缺血再灌注损伤具有保护作用,其机制与通过下调Caspase-3基因表达抑制心肌缺血再灌注损伤诱导的细胞凋亡有关。
Objective：To study the effect and mechanism of（breviscapine,bre）on myocardial apoptosis induced by ischemia-reperfusion injury in rat.Methods：Myocardial Ischemia reperfusion injury model was established by ligating the left descend coronary artery（LDA）.40 SD rats were randomly divided into control group,ischemia reperfusion（IR）group and breviscapine group.Rats in breviscapine group were injected with breviscapine 25、50mg·kg-1·d-1 respectively prior to ischemia/reperfusion.Other two groups were given NS instead of breviscapine equally at a week before the operation.After ischemia 30 min and reperfusing 2 hours,The apoptosis index of cardiomyocyte was detected by TUNEL.The level of Caspase-3 protein was determined by western blotting.Result：Apoptosis index（AI） and the level of Caspase-3 protein in IR group was higher significantly than those of control group（P0.01）,but in breviscapine group they decreased（P0.05,P0.01）.Conclusion： Breviscapine can protect the myocardium from ischemia-reperfusion injury.The mechanism is that breviscapine inhibit the myocardial apoptosis induced by ischemia reperfusion by downregulating the protein expression of caspase-3 gene.
出处
《中国中医基础医学杂志》
CAS
CSCD
北大核心
2011年第5期517-519,共3页
JOURNAL OF BASIC CHINESE MEDICINE
基金
河北省教育厅资助项目(038701)
