中文摘要：

目的观察血红素加氧酶-1（hemeoxygenase-1,HO-1）对链脲佐菌素（streptozotocin,STZ）诱导的糖尿病心肌病（diabeticcardiomyopathy,DCM）的保护作用并探讨其相关分子机制。方法对出生8w的雄性HO-1转基因小鼠和同笼阴性小鼠连续5次腹腔注射STZ（50mg/kg）,以血糖≥16.7mmol/L作为糖尿病模型入选标准,常规饲养8w,期间每周检测小鼠血糖、饮水量、进食量、尿量和体重,小鼠取材前利用超声心动图检测小鼠左室心脏功能。断颈处死小鼠后取左室心肌并进行电镜和病理组织学检查;用qRT-PCR法检测心肌ANP、BNPmRNA表达情况。并对相关数据作统计学分析。结果超声心动图检查发现,与对照组小鼠相比糖尿病组小鼠均存在心脏功能障碍,过表达HO-1的糖尿病小鼠左室心脏功能明显好于糖尿病小鼠;HE染色和透射电镜结果显示糖尿病小鼠心肌结构紊乱,线粒体损伤明显;过表达HO-1糖尿病小鼠心肌结构和线粒体结构紊乱情况改善。相对于对照组小鼠,糖尿病小鼠心肌中ANP和BNPmRNA表达升高,过表达HO-1糖尿病小鼠心肌中ANP和BNPmRNA表达降低。结论HO-1可改善由糖尿病引起的心脏功能障碍和心肌结构损伤。

英文摘要：

Objective To determine the molecular mechanism of the Heme Oxygenase-1（ HO-1） plays a major protective role in streptozotocin（ STZ） induced diabetic cardiomyopathy（ DCM）. Methods The diabetic mouse model was induced by consecutive peritoneal injections of STZ（ 50 mg / kg）. Blood glucose levels≥16. 7mmol / L were defined as diabetes and routinely feed for 8 w. In the whole experiment process,the blood glucose,water intake,food intake,urine volume and body weight of the mice were monitored. The left ventricular function of the mice was detected by echocardiography. The mice were sacrificed by cervical dislocation and then the left ventricular myocardial was removed. The left ventricular myocardial was observed by electron microscopy and histopathological detection.The expression of ANP and BNP mRNA in the myocardium was detected by qRT-PCR. The Data were analyzed by statistics. Results Compared with the control group,there was a left ventricular cardiac dysfunction in the diabetic mice and overexpression of HO-1 was appeared in the control group than those in diabetic mice. Overexpression of HO-1 was alleviated myocardial structure changes. Myocardial ANP and BNP mRNA were decreased in HO-1overexpressed mice compared with diabetic mice. Conclusion HO- 1 can improve cardiac dysfunction and myocardial structural damage in DCM.