红芪多糖对糖尿病大鼠心肌纤维化的影响及其潜在机制.docVIP

  红芪多糖对糖尿病大鼠心肌纤维化的影响 及其潜在机制# 张晓敏1，何继瑞2，李洁1，徐坤2** 5 10 （1. 兰州大学第二临床医学院，兰州 730000； 2. 兰州大学第二医院内分泌与代谢临床医学中心，VIP 糖尿病科，兰州 730030） 摘要：目的 探讨红芪多糖对 2 型糖尿病大鼠心肌纤维化的影响及可能机制。方法 采用高 脂高糖饲料加单次腹腔注射链脲佐菌素（30mg/kg）制备 2 型糖尿病大鼠模型。大鼠分为正 常对照组（NC 组）、糖尿病组（DM 组）及红芪多糖组（HPS 组）3 组，每组 10 只，干预 8 周后所有大鼠称重，计算心重指数。实时荧光定量 PCR 法（Real-time quantitative PCR） 测定心肌局部 TGF-β1、Smad3、Smad7 mRNA 水平，免疫组化法测定 TGF-β1、Smad3、 Smad7 蛋白水平，透射电镜下观察大鼠心肌超微结构，Masson 染色测定心肌胶原含量。结 果 与 NC 组比较，DM 组、HPS 组心肌胶原含量增多，间质纤维化明显，H/B、TGF-β 15 1、Smad3 表达均明显升高，Smad7 表达降低（P＜0.01）；与 DM 组比较，HPS 组大鼠心肌 纤维化减轻，H/B、TGF-β1、Smad3 表达下降，Smad7 表达有所升高（P＜0.05）。心肌 病理改变：与 NC 组相比，DM 组大鼠心肌胶原纤维明显增多，排列紊乱，线粒体肿胀；而 HPS 干预组上述改变减轻。结论 红芪多糖通过抑制 TGF-β1/Smads 信号通路，延缓了糖 尿病大鼠心肌纤维化的发生和发展。 20 25 30 35 关键词：2 型糖尿病；红芪多糖；心肌纤维化；转化生长因子β1；smad3；smad7 中图分类号：R587.1 Effect of Hedysarum Polybotys Saccharide on myocardial fibrosis in diabetic rats Zhang Xiaomin1, HE Jirui2, Li Jie1, Xu Kun2 (1. School of Second Clinical Medicine of Lanzhou University,Lanzhou 730000; 2. The Endocrinology and Metabolism Center,The VIP Diabetes Department of the Second Hospital of Lanzhou University,Lanzhou 730030) Abstract: Objective To investigate the effect of Hedysarum Polybotys Saccharide（HPS） on myocardial fibrosis in diabetic rats and its underlying mechanism. Methods Type 2 diabetic animal models was established by feeding high-sucrose and high-fat diet and intraperitoneal injecting low dose streptozotocin（30mg/kg）.After the success of modeling,diabetic rats were divided into three groups:normal control group（NC group）,diabetes group（DM group）and Hedysaryum Polybotys Saccharide group（HPS group）. There are ten rats in each group.After 8 weeks，we weighted all rats and calculated the heart body weight ratio(H/B),Real-time quantitative PCR was used to estimate the levels of TGF-β1,Smad3,Smad7 mRNA in mycardium. The expression of myocardial TGF-β1,Smad3,Smad7 protein was determined by immunohistochemistry. Myocardial pathologic changes were observed under transmission electronic