Key result
Oxymatrine significantly ameliorated hemodynamics, inhibited TβR(1) and Smad3 mRNA expression, and reduced left ventricle weight/body weight in rats with acute myocardial infarction.
Why the study?
Does oxymatrine improve hemodynamics and reduce myocardial fibrosis in rats with acute myocardial infarction?
RCT
randomly assigned
Does oxymatrine improve hemodynamics and reduce myocardial fibrosis in rats with acute myocardial infarction?
Oxymatrine demonstrates a protective effect against myocardial fibrosis in a rat model of acute myocardial infarction, likely by modulating the TGF-β1-Smads signaling pathway.
Caution against clinical use post-MI; leaves open translation of antifibrotic effects to human trials.
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-β(1))-Smads signaling pathways. Rats with AMI induced by ligation of left anterior descending branch were randomly assigned to receive 1 50 and 25 mg/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 24 h after infarction had been investigated based on (1) hemodynamics, (2) tissue weights, (3) biochemical indicator (hydroxyproline contents in left ventricle), and (4) TGF-β(1), TGF-β(1) receptor (TβR(1)), Smad3, Smad4, Smad7, Col1, and Col3 expression by semi-quantitative reverse transcription PCR. Treatment with 1 significantly ameliorated hemodynamics, inhibited the expression of TβR(1) 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-β(1)-Smads signal pathway.
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Shen et al. (2011) conducted an RCT in myocardial fibrosis induced by acute myocardial infarction. Oxymatrine vs. model group, sham-operated group, and captopril group was evaluated on hemodynamics, tissue weights, hydroxyproline contents, and TGF-β(1)-Smads signaling pathway expression. Oxymatrine significantly ameliorated hemodynamics, inhibited TβR(1) and Smad3 mRNA expression, and reduced left ventricle weight/body weight in rats with acute myocardial infarction.
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