心达康片对心肌缺血再灌注损伤模型大鼠的保护作用研究  

Protective Effects of Xindakang Tablets on Myocardial Ischemia-reperfusion Injury Model Rats

作　　者：曾碧映 曾嵘[2] 李新才 邓凤君 李学军 梁娟[3] 孙淑纯 周利 廖端芳[2] 

机构地区：[1]湖南益阳医学高等专科学校,湖南益阳413000 [2]湖南中医药大学,长沙410208 [3]湖南省妇幼保健院,长沙410008 [4]湖南湘潭市中医院药剂科,湖南湘潭411100

出　　处：《中国药房》2013年第31期2902-2904,共3页China Pharmacy

摘　　要：目的:研究心达康片对心肌缺血再灌注损伤模型大鼠的保护作用。方法:采用结扎冠状动脉左前降支30min后再灌注120min的方法复制大鼠心肌缺血再灌注损伤模型。实验分为假手术(等容生理盐水)组、模型(等容生理盐水)组、盐酸地尔硫(14mg/kg)组与心达康高、中、低剂量(6、4、2mg/kg)组,灌胃给药,给药7d后复制模型。检测大鼠血清乳酸脱氢酶(LDH)、肌酸激酶(CK)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性与心肌细胞中三磷酸腺苷(ATP)酶活性;免疫组化法测定B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)的表达。结果:与假手术组比较,模型组大鼠血清中CK、LDH活性显著增强,SOD和GSH-Px活性显著减弱,心肌细胞ATP酶活性显著减弱,Bax表达显著增强,Bcl-2表达显著减弱(P<0.01);与模型组比较,心达康高、中、低剂量组大鼠血清中CK、LDH活性显著减弱,SOD和GSH-Px活性显著增强,心肌细胞ATP酶活性显著增强,Bax表达显著减弱,Bcl-2表达显著增强(P<0.01或P<0.05)。结论:心达康片对心肌缺血再灌注损伤模型大鼠具有明显的保护作用,其机制可能与其增强机体清除自由基能力,改善心肌细胞ATP酶的能量代谢,以及抑制心肌缺血后心肌细胞凋亡有关。OBJECTIVE： To study the protective effects of Xindakang tablets on myocardial ischemia-reperfusion injury （MIRI） model rats. METHODS： M1RI model was induced by 120 min reperfusing 30 min after ligating the left anterior descending coronary artery. Model rats were divided into sham operation group （constant volume of normal saline）, model group （constant vol- ume of normal saline）, Hexinshuang group（14 mg/kg） and Xindakang high-dose, medium-dose and low-dose groups （6, 4, 2 mg/ kg）. They were given medicine intragastrically for 7 days. The activities of LDH, CK, SOD and GSH-Px in serum and the activity of ATP in myocardial cells were determined. The expressions of Bcl-2 and Bax in myocardial cells were determined by immunohis- tochemical staining. RESULTS ： Compared with sham operation group, the activities of CK and LDH were increased while those of SOD and GSH-Px were decreased significantly in model group;while the activity of ATP and the expression of Bcl-2 in myocardial cells were decreased significantly and the protein expression of Bax was increased significantly （P〈0.01）. Compared with model group, the activities of CK and LDH in serum in Xindakang high-dose, medium-dose and low-dose groups were decreased signifi- cantly, while the activities of SOD and GSH-Px were increased significantly; the activity of ATP and the expression of Bcl-2 in myocardial cells were increased significantly, while the protein expression of Bax was decreased significantly （P〈0.01 or P〈 0.05）. CONCLUSIONS： Xindakang tablets could protect against MIRI in rats. The potential mechanism is related to enhance func- tion of eliminating free radical, improving the metabolism ofATPase, and attenuating cardiomyocyte apoptosis.

关 键 词：心达康片 心肌缺血再灌注损伤 细胞凋亡 

分 类 号：R285[医药卫生—中药学] R541[医药卫生—中医学]