水杉总黄酮抗实验性心肌肥厚作用的研究  

Inhibitory effects of total flavones metasequosia on experimental cardiac hypertrophy

作　　者：杨晓茹[1] 刘惟莞[1] 石明健[1] 王红英[1] 敖英[1] 

机构地区：[1]湖北医科大学药理学教研室,武汉430071

出　　处：《中国药理学通报》2000年第1期87-89,共3页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助课题!No39770088

摘　　要：目的　研究水杉总黄酮对实验性心肌肥厚的作用及其机制。方法　采用腹腔动 静脉造瘘建立大鼠容量超负荷心肌肥厚模型 ,水杉总黄酮灌胃给药 ,持续 5wk后 ,测定心室肌细胞内Ca2 +浓度、血浆和心肌AngⅡ、心肌MDA及SOD。结果　水杉总黄酮剂量依赖性地减轻大鼠心脏重量 ,抑制心室RNA和蛋白质合成 ,降低心室肌细胞内Ca2 +浓度和心室AngⅡ、MDA含量 ,增加SOD活性。 结论　水杉总黄酮可预防容量超负荷大鼠心肌肥厚的形成 ,其机制可能与拮抗心脏局部RAS ,减轻Ca2AIM To investigate the effects of total flavones of metasequosia(TFM) on experimental cardiac hypertrophy and its mechanismMETHODS Volumeoverload cardiac hypertrophy of rats were induced by aortocaval shunts The rats were given ig TEM (400,40 and 4 mg·kg -1 ·d -1 ) for 5 wk after operationThe concentration of free calcium in the isolated ventrcular cells,the content of AngⅡ and MDA,and the activity of SOD were measured respectively RESULTS TFM reduced the radios of VW/BW and contents of RNA and protein in the myocardium, decreased the concentration of free calcium in the isolated ventrcular cells and the content of myocardial AngⅡ and MDA,increased the activity of SOD in dosedependent mannerCONCLUSION TFM can prevent volumeoverload induced cardiac hypertrophy in ratsThe effects may be related to its action of antagonizing RAS and oxidation and reducing Ca 2+ overload

关 键 词：水杉总黄酮 心肌肥厚 实验研究 

分 类 号：R542.2[医药卫生—心血管疾病] R972[医药卫生—内科学]