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麝香保心丸对糖尿病大鼠心肌纤维化的影响
引用本文:刘小燕,王远征,韩玉.麝香保心丸对糖尿病大鼠心肌纤维化的影响[J].中药药理与临床,2012(1):28-31.
作者姓名:刘小燕  王远征  韩玉
作者单位:辽宁医学院;中国人民解放军第205医院
摘    要:目的:探讨麝香保心丸对糖尿病(DM)大鼠心肌纤维化的影响。方法 :40只SD大鼠随机分为正常对照组、糖尿病模型组、麝香保心丸(50mg/kg、100mg/kg),每组10只,给药12周后称量体重及全心、左室重量,计算心体比(H/B)和左室重量指数(LVMI);Masson染色测量心肌间质胶原容积分数(CVF);电镜观察心肌细胞超微结构;放射免疫法测定心肌局部血管紧张素Ⅱ(AngⅡ)的浓度;免疫组化法测定转化生长因子-β1(TGF-β1)的表达情况。结果:糖尿病模型组H/B、LVMI增高;心肌间质CVF增高;心肌纤维排列紊乱,线粒体肿胀,堆积。TGF-β1的表达、AngⅡ的浓度明显上调。麝香保心丸(50mg/kg、100mg/kg)上述趋势均明显好转,并且具有剂量依赖性,高剂量组改变更明显。结论:麝香保心丸可以抑制糖尿病大鼠心肌纤维化,机制可能与降低TGF-β1、AngⅡ的表达有关。

关 键 词:麝香保心丸  糖尿病  心肌纤维化  转化生长因子-β1  血管紧张素Ⅱ

Effect of Shexiangbaoxinwan Pill on myocardial fibrosis of diabetic rats
Liu Xiaoyan,Wang Yuanzheng,Han Yu.Effect of Shexiangbaoxinwan Pill on myocardial fibrosis of diabetic rats[J].Pharmacology and Clinics of Chinese Materia Medica,2012(1):28-31.
Authors:Liu Xiaoyan  Wang Yuanzheng  Han Yu
Institution:1 (1 Liaoning Medical University;2 205 Hospital of PLA,Jinzhou 121001) Objective: To investigate the effects of ShexiangbaoXinwan(SBW) on myocardial fibrosis of diabetic rats.Methods : Forty SD rats were randomly divided into the normal control group,the diabetic group,the diabetic group treated with low dose shexiangbaoxinwan(50mg/kg)and the diabetic group treated with high dose shexiangbaoxinwan(100mg/kg),Rats in the last two groups were fed with shexiangbaoxinwan for 12 weeks.After the rats were killed,body weight,heart weight and left ventricular mass were weighted.The ratio of heart weight to body weight(H/B) and left ventricular mass index(LVMI) were calculated.The myocardial interstitial collagen volume fraction(CVF) were Measured with Masson methods.The ultrastructure of myocardial cell was observed with electron micscope.The concentration of AngiotensinII(AngII) of regional myocardium were determined by radioimmunoassay.The expressions of TGF-β1 were determined by immunohistochemistry.Results Compared with the NC group,H/B,LVMI and myocardial interstitial CVF increased in the DM group.rats in the DM group had abnormal cardiac ultrastructure with confusion of my-ofibril and swelling and gathering of mitochondria.Expression of TGF-β1 and the concentration of AngII obviously increased.The above trends were significantly improved in the last two groups,and have a dose-dependent,High-dose group changes more obvious.Conclusion : Shexiangbaoxinwan Pill can inhibit diabetic myocardial fibrosis in rats,the mechanisms may relate with reducing the expression of TGF-β1 and AngⅡ.
Abstract:Objective: To investigate the effects of ShexiangbaoXinwan(SBW) on myocardial fibrosis of diabetic rats.Methods : Forty SD rats were randomly divided into the normal control group,the diabetic group,the diabetic group treated with low dose shexiangbaoxinwan(50mg / kg) and the diabetic group treated with high dose shexiangbaoxinwan(100mg / kg),Rats in the last two groups were fed with shexiangbaoxinwan for 12 weeks.After the rats were killed,body weight,heart weight and left ventricular mass were weighted.The ratio of heart weight to body weight(H / B) and left ventricular mass index(LVMI) were calculated.The myocardial interstitial collagen volume fraction(CVF) were Measured with Masson methods.The ultrastructure of myocardial cell was observed with electron micscope.The concentration of AngiotensinII(AngII) of regional myocardium were determined by radioimmunoassay.The expressions of TGF-β1 were determined by immunohistochemistry.Results Compared with the NC group,H / B,LVMI and myocardial interstitial CVF increased in the DM group.rats in the DM group had abnormal cardiac ultrastructure with confusion of my-ofibril and swelling and gathering of mitochondria.Expression of TGF-β1 and the concentration of AngII obviously increased.The above trends were significantly improved in the last two groups,and have a dose-dependent,High-dose group changes more obvious.Conclusion : Shexiangbaoxinwan Pill can inhibit diabetic myocardial fibrosis in rats,the mechanisms may relate with reducing the expression of TGF-β1 and AngⅡ.
Keywords:Shexiangbaoxin Pill(麝香保心丸)  diabetic mellitus  myocardial fibrosis  TGF-β1  AngⅡ
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