血管紧张素抑制剂对糖尿病心脏损伤的保护机制
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[摘要] 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。
[关键词] 2型糖尿病；血管紧张素II；心脏
[中图分类号]R587.2 [文献标识码] A [文章编号] 1673-9701(2011)19-12-04
Protection Mechanism of Angiotensin Inhibitors on Cardiac Injury in Rats with Diabetes
ZHANG ZhongYANG YanhongJIAO Xiangying
Anatomic Department, Cytophysiology Key Laboratory ofShanxi Medical University of Common Foundation by Shanxi Province and Ministry of Education , Taiyuan 030001,China
[Abstract] Objective To studytheprotection mechanism of angiotensin inhibitors on cardiac injury in rats withtype 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 gavage, 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 Ⅰ (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, cTn1, MDA were significantly decreased, SOD significantly increased ......
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