葛根素对心肌缺血再灌注损伤大鼠心肌酶的影响

目的观察葛根素对心肌缺血再灌注损伤大鼠心肌酶的影响。方法以雄性Wistar大鼠为研究对象,将实验动物分为5组即假手术组、心肌缺血再灌注模型组（I/P）、葛根素2mg/Kg给药组（A组）、葛根素5mg/Kg给药组（B组）和葛根素10mg/Kg给药组（C组）。采用结扎大鼠冠状动脉左前降支（LAD）的方法,建立大鼠心肌缺血再灌注损伤模型;观察各组大鼠心肌梗死的面积及心肌酶的变化。结果与假手术组比较,I/P组大鼠的心肌梗死面积明显增大、心肌酶学各指标均发生显著变化,差异均有统计学意义（P〈0.01）;与I/P组比较,葛根素各剂量组均降低了心肌缺血再灌注损伤大鼠的心梗面积,减少了心肌细胞磷酸肌酸激酶（CK）、乳酸脱氢酶（LDH）释放、心肌组织黄嘌呤氧化酶（XO）活性及血清丙二醛（MDA）含量,提高了血清一氧化氮（NO）水平、血清超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性及谷胱甘肽（GSH）含量,差异有统计学意义（P〈0.01）,并存在剂量反应关系。结论葛根素对心肌缺血再灌注损伤模型大鼠具有抗氧化应激作用,能够减轻心肌酶学的改变,从而减少心肌梗死面积,并存在剂量反应关系。

Effect of Puerarin on myocardial ischemia-reperfusion injury in rat cardiac enzymes

Objective To observe the effect of puerarin on myocardial ischemia-reperfu sion injury in rat cardiac en zymes. Methods Male Wistar rats were randomly divided into sham group, myocardial ischemia-reperfusion model group, the puerarin 2 mg/Kg dose group（A）, the the puerarin 5 mg/Kg dose group（B）, the the puerarin 10mg/Kg dose group（C）. Ligation of left anterior descending coronary artery（LAD） ,the establishmen-t of myocardial ischemia-reper- fusion injury model;Rats myocardial infarct size and myocardial enzyme changes were observed. Results Myocardial in- farct size compared with the sham group, I/P rats significantly increased serum creatine kinase targets were a significant change,the differences were statiscally significant （P〈0. 01）;compared with the I/P group, Puerariahormone dose group were reduced myocardial ischemivre-perfusion injury in rat infarct size,reduce of cardiomyocytes phosphate crea- tine kinase（CK）,lactate dehydrogenase（LDH） release,myocardial tissue xanthine oxidase（XO）activity and serum ma- londialdehyde（MDA）,increased serum nitric oxide（NO）levels, serum superoxide dismutase（SOD）, glutathione peroxi- dase（GSH-Px） activity and glutathionepeptide（GSH）, the difference was statistically significant（P〈0.01）, and the ex- istence of a dose-response relationship. Conclusion Puerarin on myocardial isch-emia-reperfusion injury model in rats with anti -oxidative stress effect can reduce the changes of serum crestine kinase, thereby reducing myocardial infarct size,and presence of a dose-response relationship.