黄芩茎叶总黄酮预处理对大鼠心肌缺血再灌注损伤的保护作用

Protective effects of scutellaria baiculensis stem-leaf total flavonoid pretreatment against myocardial ischemia/reperfusion injury in rats

目的探讨黄芩茎叶总黄酮(Scutellaria baiculensis stem-leaf total flavonoid,SSTF)对大鼠心肌缺血再灌注损伤的保护作用。方法40只SD大鼠随机分为假手术组、缺血再灌注组和SSTF预处理组。SSTF组大鼠于术前1周分别灌胃不同剂量的SSTF〔(17.5、35、70mg/(kg.d)〕,另两组给等量生理盐水。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。缺血30min、再灌注2h后,观察大鼠心电图的变化;并用免疫组织化学法检测心肌组织中Bax和Bcl-2蛋白表达情况。结果SSTF抑制了缺血再灌注损伤大鼠心电图T波升高,降低了心律失常发生率。缺血再灌注组Bcl-2蛋白表达阳性细胞率明显比假手术组低(P<0.05),Bax蛋白表达阳性细胞率明显较假手术组高,而SSTF预处理组Bcl-2蛋白表达阳性细胞率明显高于缺血再灌注组(P<0.05),Bax蛋白表达阳性细胞率明显较缺血再灌注组为低(P<0.05)。结论SSTF预处理对缺血再灌注的心肌细胞具有保护作用,其机制可能与上调Bcl-2和下调Bax蛋白表达进而抑制心肌细胞凋亡有关。

Objective To investigate protective effects of scutellaria baiculensis stem-leaf total flavonoid pretreatment against myocardial ischemia/reperfusion injury in rats. Methods Fourty SD rats were divided into sham operation group, ischemia/reperfusion group and SSTF pretreatment group at random. Rats of SSTF group were perfused with SSTF 17.5,35,70mg/（kg· d） respectively prior to ischemia/reperfusion. Other two groups were given NS instead of SSTF equally a week before the operation. Myocardial ischemia reperfusion injury model was established by ligating the left descend coronary artery （LDA） 30 min and reperfusing 2h. After operation the cardiac function of rats were observed. The expression of Bcl-2 and Bax protein were detected by immunohistochemical stain. Results SSTF pretreatment inhibited the increasing of T wave after ischemia reperfusion damage and decreased the occurrence of arrhythmias. The positive rate of Bcl-2 expression was significantly decreased in I/R than that in SO（ P 〈 0.05） ,while Bax expression cells were significantly higer in I/ R than those in SO（ P 〈 0.05）, but the positive rate of Bcl-2 expression was significantly increased in SSTF than that in I/R group （P 〈 0.05）, while Bax expression ceils were significantly lower in SSTF than those in I/ R（ P 〈 0.05）. Conclusion SSTF has the protective effect of myocardial ischemia reperfusion, and its mechanism may be associated with up-regulating protein expression of bel-2 gene and down-regulating protein expression of bax gene.