Protective effect of oxymatrine on myocardial fibrosis induced by acute myocardial infarction in rats involved in TGF-1-Smads signal pathway
Protective effect of oxymatrine on myocardial fibrosis induced by acute myocardial infarction in rats involved in TGF-1-Smads signal pathway
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DOI：
10.1080/10286020.2010.550883
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发表时间：
2011-01-01
影响因子：
1.7
通讯作者：
Liu, Xing-De
中科院分区：
文献类型：
--
作者：
Shen, Xiang-Chun;Yang, Yu-Ping;Liu, Xing-De
氧化苦参碱(1)是从传统中药苦参（Sophora japonica, Sophora flavescens Ait.）中提取的一种成分，已被证明具有多种药理作用。大量实验证据表明，1可能对心血管系统有保护作用。本研究旨在探讨1对急性心肌梗死（AMI）诱导的心肌纤维化的可能作用及其对转化生长因子-1 (TGF-1)-Smads信号通路的调节。左前降支结扎致AMI大鼠，随机分为1 50、25mg/kg ig，模型组与假手术组比较，阳性组用卡托普利治疗。根据(1)血流动力学、(2)组织重量、(3)生化指标（左心室羟脯氨酸含量）、(4)TGF-1、TGF-1受体（TR1）、Smad3、Smad4、Smad7、Col1、Col3半定量反转录PCR表达情况，研究梗死后24小时开始1周治疗的效果。1治疗显著改善了血流动力学，抑制了TR1 mRNA和Smad3 mRNA的表达，降低了左心室重量/体重。本研究结果提示1可能具有抗心肌纤维化的作用，其机制可能与调节TGF-1-Smads信号通路有关。
Oxymatrine (1), a component extracted from a traditional Chinese herb Sophora japonica (Sophora flavescens Ait.), has been demonstrated to have a variety of pharmacological actions. Abundant experimental evidence indicates that 1 may exert a protective effect on the cardiovascular system. This study was designed to explore the possible role of 1 against myocardial fibrosis induced by acute myocardial infarction (AMI) and its modulation on transforming growth factor beta 1 (TGF-1)-Smads signaling pathways. Rats with AMI induced by ligation of left anterior descending branch were randomly assigned to receive 1 50 and 25mg/kg intragastrically, and model group which were further compared with sham-operated group, and positive group treated with captopril. The effects of 4-week therapy with 1 starting 24h after infarction had been investigated based on (1) hemodynamics, (2) tissue weights, (3) biochemical indicator (hydroxyproline contents in left ventricle), and (4) TGF-1, TGF-1 receptor (TR1), Smad3, Smad4, Smad7, Col1, and Col3 expression by semi-quantitative reverse transcription PCR. Treatment with 1 significantly ameliorated hemodynamics, inhibited the expression of TR1 mRNA and Smad3 mRNA, and reduced the left ventricle weight/body weight. The results of this research indicated that 1 might protect against myocardial fibrosis and the mechanism may be involved in modulating TGF-1-Smads signal pathway.