SMAD3,SMAD7在糖尿病大鼠心肌组织的表达

Expressions of SMAD3 and SMAD7 in the myocardial tissue of diabetic rats

目的探讨糖尿病大鼠心脏SMAD3和SMAD7的表达变化及其与糖尿病心肌病的关系。方法20只雄性SD大鼠随机分成对照组和糖尿病组,腹腔注射链脲菌素建立糖尿病模型。多导生理记录仪测定大鼠心功能,测定大鼠体质量、心脏质量并计算心脏质量/体质量,电镜观察心肌超微结构改变,苦味酸天狼星染色观察心肌间质纤维化程度,原位细胞凋亡检测法(TUNEL)检测心肌细胞凋亡情况,RT-PCR测定各组大鼠的SMAD3、SMAD7的mRNA水平,免疫组化法检测SMAD3、SMAD7的蛋白水平。结果与对照组相比,糖尿病大鼠心功能受损;HW/BW明显增高(P<0.01),电镜显示心肌肌丝溶解、断裂,间质胶原增生,VG染色显示心肌间质明显纤维化(P<0.01),心肌细胞凋亡增加(P<0.01);心脏SMAD3的mRNA表达增加(P<0.01),SMAD7的mRNA表达减少(P<0.01),SMAD3蛋白表达水平增加(P<0.01),SMAD7的蛋白表达水平降低(P<0.01)。结论SMAD s信号通路活化可能参与了糖尿病大鼠心肌病的发生发展过程。

Objective To explore the change of SMAD3 and SMAD7 expression on diabetic rats＇ myocardium tissue and the relationship between the alterations with diabetic cardiomyopathy. Methods 20 male SD rats were randomly divided into control group and diabetes group, and diabetic rat model was induced by a single intraperitoneal injection of streptozotoein （STZ, 60 mg/kg）. Rats body weight （BW） and heart weight （HW） were tested and calculated HW/BW. Biodynamie recorder was used to detect the cardiac function. The changes of myocardium uhrastructure were observed by microscope. Collagen content was observed by VG staining and myocardial apoptosis was detected by TUNEL The mRNA expression levels of SMAD3 and SMAD7 were determined by RT-PCR. The protein expression levels of SMAD3 and SMAD7 were detected by immunohistochemistry. Results Compared with control group, diabetic rats experienced markedly myocardium damage： cardiac function were impaired and HW/BW was higher （P 〈0. 01 ）. Electron microscope showed myocardium myofilament was dissolved and broken and mesenehymal collagen proliferated. Myocardium mesenchyme fibrosis was found by VG staining （ P 〈 0.01 ） and myocardial cell apoptosis index was higher in diabetes group （ P 〈 0.01 ）. The expression of SMAD3 mRNA was higher and the expression of SMAD7 mRNA was lower in diabetic rat＇s heart （all P 〈 0. 01 ）. The expression of SMAD3 protein was higher and the expression of SMAD7 protein was lower in diabetic rat＇s heart （ all P 〈 0. 01 ）. Conclusions SMADs signal passage activation may participate in the progression of diabetic rat cardiomyopathy.