血管紧张素抑制剂对糖尿病心脏损伤的保护机制  被引量:1

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

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作  者:张忠[1,2] 杨艳宏[1,2] 焦向英[1,2] 

机构地区:[1]山西医科大学解剖教研室 [2]山西医科大学细胞生理学省部共建教育部重点实验室,山西太原030001

出  处:《中国现代医生》2011年第19期12-15,共4页China Modern Doctor

基  金:国家自然科学基金资助项目(30800399);山西省回国留学人员科研项目(2009-46);留学回国人员科研启动基金(2009-1341)

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。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.

关 键 词:2型糖尿病 血管紧张素Ⅱ 心脏 

分 类 号:R587.2[医药卫生—内分泌]

 

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