低剂量STZ和L-NAME联合高脂饮食诱导的代谢综合征大鼠心肌纤维化

目的 建立大鼠代谢综合征(MS)模型并了解其心功能和心肌组织结构的变化特征,为其干预治疗研究提供实验平台.方法 雄性SD大鼠尾静脉推注20 mg/kg STZ后高脂饲料喂养6周并予0.04%L-NAME 和10%果糖混合溶液饮用,观察大鼠MS基本特征的变化.6周后处死大鼠并采用离体心脏功能实验评价心功能,HE染色及免疫...

Myocardial fibrosis of metabolic syndrome rats induced by low dose of STZ and L-NAME with high-fat diet

Objective To establish a rat model of metabolic syndrome and investigate the changes in cardiac function and cardiomyopaphy of the model, and to supply an experimental platform for the therapeutic study. Methods Male SD rats were fed with a high-fat diet for 6 weeks after being administered 20 mg/kg STZ through tail intravenous injection, and were given with 0.04% L-NAME solution mixed with 10% fructose through daily drinking. The change of metabolism syndrome basic characteristics was observed and recorded. Isolated heart function test was employed to determine the cardiac function of the rats. The myocardium pathological section was stained by HE and the expressions of Collagen Ⅰ and Collagen Ⅲ in myocardial tissue were detected by immunofluoreseenee. Results Blood pressure and plasma triglyceride, high-density lipoprotein and LDL/HDL levels of the treated rats were all increased significantly after 3 weeks （ P 〈 0.05 ）. The fasting plasma glucose and AUC of oral glucose tolerance test of treated group increased （ P 〈 0.05 ） after 6 weeks. The heart rate, LVPP, LVDP, - dp/dt max and Vpm of the treated rats all decreased but LVEDP increased significantly （ P 〈 0.05 ）. By staining,broken junctions and wide gaps between muscle fibers were observed in the myocardium of the treated rats, expression of Collagen m increased significantly while expression of Collagen I didnl change obviously. Conclusion Myocardial fibrosis, cardiac dysfunction and other typical changes of metabolic syndrome with high blood pressure,high glucose and lipid could be induced in treated rats with high-fat diet, which could be applied as an ideal animal model for the study of cardiac diseases in MS.