血管紧张素抑制剂对糖尿病心脏损伤的保护机制

Protection Mechanism of Angiotensin Inhibitors on Cardiac Injury in Rats with Diabetes

目的本课题旨在研究2型糖尿病大鼠心脏血管紧张素II的变化及其影响,并探讨其机制。方法将雄性SD(Sprague Dawley)大鼠分为两组,糖尿病组高糖高脂喂养,用小剂量(40mg/kg)链唑霉素腹腔注射诱导成为2型糖尿病大鼠模型;对照组普通饲料喂养,腹腔注射柠檬酸缓冲液;再将糖尿病组分为两组,一组灌胃生理盐水(0.5mL/(kg.d),一组灌胃雷米普利水溶液(1mg/(kg.d),灌胃8周后,检测心功能的各项参数指标,测定血浆与心肌组织中血管紧张素II(AngⅡ)的含量,测定心肌Caspase-3活性,测定血清肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白I(cTnI)含量,测定心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)含量。结果同对照组比较,2型糖尿病组血浆与心肌组织中的AngII含量明显升高,心功能LVSP、dp/dtmax明显下降、LVEDP明显升高,Caspase-3、CK-MB、cTnI、MDA均明显升高,SOD明显降低;与灌胃生理盐水组相比,灌胃雷米普利组血浆与组织中AngII含量明显降低,心功能dp/dtmax明显升高、LVEDP明显降低,Caspase-3、CK-MB、cTnI、MDA均明显降低,SOD明显升高。结论血管紧张素II升高参与了糖尿病时髙糖高脂所介导的心脏功能受损、心肌细胞损伤,因此通过对AngII的抑制,可以对2型糖尿病引起的心脏损伤起到一定的保护作用。

Objective To study the protection mechanism of angiotensin inhibitors on cardiac injury in rats with type 2 diabetes. Methods Male Sprague Dawley （SD） rats were divided into two groups, high-sugar high-fat fed diabetic group, with a small dose （40 mg / kg ） intraperitoneal injection of streptozotocin induced rat model of type 2 diabetes to become; control group of ordinary diet, intraperitoneal injection of citrate buffer; Diabetic group and then divided into two groups, one group was given normal saline （ 0.5mL/ （kg · d ））, one group was given ramipril solution （1mg/（kg · d ））, eight weeks after garage, test heart function The parameters and measured plasma and cardiac tissue angiotensin Ⅱ （ Ang Ⅱ ） content of myocardial Caspase-3 activity, serum creatine kinase （ CK- MB ）, cardiac troponin （ cTnI ） Content of myocardial superoxide dismutase （SOD）, malondialdehyde （MDA） content. Results The Results showed that compared with the control group, type 2 diabetes, plasma and myocardium Ang Ⅱ was significantly higher in heart function LVSP, dp/dtmax decreased, LVEDP increased significantly, Caspase-3, CK-MB, cTn1, MDA were significantly increased, SOD significantly decreased; and intragastric saline group, fed the blood ramipril award and tissue Ang Ⅱ were significantly decreased heart function dp/dtmax increased significantly, LVEDP decreased, Caspase -3, CK-MB, cTnl, MDA were significantly decreased, SOD significantly increased. Conclusion Angiotensin Ⅱ increased in the diabetes high glucose and lipid-mediated impaired heart function, myocardial cell damage, through inhibition of Ang Ⅱ may be due to type 2 diabetes, heart damage play a protective role.