冠心康对缺血再灌注损伤大鼠心肌细胞形态结构和Caspase-3活性的影响

Effect of “Guanxinkang” on myocardial cell morphology and Caspase-3 activity in rats with ischemia reperfusion injury

目的观察冠心康对缺血再灌注损伤大鼠心肌细胞形态结构和Caspase-3活性的影响。方法将40只SD雄性大鼠随机分为假手术组、心肌缺血再灌注损伤(MIRI)模型组、冠心康组、盐酸地尔硫卓组,每组10只。冠心康组灌胃给予冠心康,盐酸地尔硫卓组灌胃给予盐酸地尔硫卓,假手术组和MIRI模型组于相同时间分别灌胃给予等容积的0.9%NaCl溶液,各组术前灌胃均每天1次,连续7天。灌胃7天后,采用结扎大鼠心脏左冠状动脉前降支30 min、再灌注2 h复制大鼠心肌缺血再灌注损伤模型。造模后,在MIRI结扎线以下区域至心尖取材,运用常规苏木素-伊红(HE)染色,光镜下用图形分析系统定量观察单位视野全部心肌细胞核染色部分的面积、积分光密度,采用生化法检测Caspase-3活性。结果 MIRI模型组大鼠心肌细胞结构破坏,冠心康组大鼠心肌细胞保持完好。与假手术组比较,MIRI模型组大鼠单位视野全部心肌细胞核染色部分的面积和积分光密度显著降低(P<0.01);冠心康组和盐酸地尔硫卓组则显著升高,与MIRI模型组比较差异有统计学意义(P<0.01);MIRI模型组大鼠心肌组织Caspase-3活性较假手术组明显升高(P<0.01),冠心康组和盐酸地尔硫卓组Caspase-3活性则较MIRI模型组明显降低(P<0.01)。结论冠心康对心肌缺血再灌注损伤大鼠心肌组织具有保护作用,其机制与冠心康抑制心肌组织Caspase-3活性有关。

Objective To observe the effect of ＂Guanxinkang＂ on myocardial （＇ell morphology and Caspase-3 activity in rats with ischemia reperfusion injuu. Methods Forty SD rats were randomly divided into sham-operation group, MIRI model group, ＂Guanxinkang＂ group and l）ihiazem Hydroehloride group, with 10 rats in each group. The ＂＇Guanxinkang＂ group was intragastrically treated with ＂Guanxinkang＂, Diltiazem Hydruchloride g^up with Dihiazem Hydrochloride. The sham-operation group and MIRI model group were intragastrically treated with the same wflmne of normal saline, with the course of 7 days befor operation, once a day. At the 7＇l＇ day after intragastrie administration,the rats models were established by ligating Ihe left anterior descending euronmy fbr 30 min and 2 h reperfusion. After modeling, the area of stained cell nucleus and inlegral optical density wer observed by light mieroscope after HE staining, and the Caspase-3 activity was detected by biochemical method. Results The structure of myocardial cells in MIRI model group were damaged, while it wer completed in ＂Guanxinkang＂ group. Compared with sham-operation group, the area of stained cell nucleus and integral optical density in MIRI model group we~ decreased significantly （P 〈 0.01 ） ; while they were increased in ＂Guanxinkang＂ group and Dihiazem Hydrochloride group, with significant difference between MIRI group and those two groups （ P 〈 0.01 ） ; the Caspase-3 activity in MIR1 group was increased and higher than that of the sham-operation group （ P 〈 0.01 ）, while the Caspase-3 activity in ＂Guanxinkaug＂ group and Dihiazem Hydrochloride group were decreased and lower than that of the MIRI group （ P 〈 0.01 ）. Conclusion ＂Guanxinkang＂ has protective effect in rats with ischemia repeffusion injury ; its mechanism may be association with restraining the Caspase-3 activity of myocardial cells.