4.4 Article

Protective effect of oxymatrine on myocardial fibrosis induced by acute myocardial infarction in rats involved in TGF-1-Smads signal pathway

期刊

JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
卷 13, 期 3, 页码 215-224

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/10286020.2010.550883

关键词

oxymatrine; acute myocardial infarction; cardiac fibrosis; TGF-1-Smads signal

资金

  1. National Natural Science Foundation of China [30701024]
  2. Provincial Key Technologies R&D Program of Guizhou [2007-1035]
  3. International Science and Technology Exchange and Cooperation of Guizhou Province [2009-700115]
  4. Foundation for Open Projects of Jiangsu Key Laboratory for Pharmacology
  5. Safety Evaluation of Chinese Materia Medica [P09003]

向作者/读者索取更多资源

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.

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