Abstract
Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-β1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-β1/Smad3 pathway.
Highlights
Myocardial ischemia is a cardinal cardiovascular disease and a major cause of morbidity and mortality worldwide [1]
The present study suggested that treatment with ginsenoside Re suppressed isoproterenol-induced myocardial fibrosis and heart failure markedly in rats
These results suggested that ginsenoside Re could ameliorate the impairment in heart function caused by myocardial ischemia
Summary
Myocardial ischemia is a cardinal cardiovascular disease and a major cause of morbidity and mortality worldwide [1]. Ischemic injury leads to the development of myocardial fibrosis due to the negligible regenerative capacity of the heart. Myocardial fibrosis is associated with increased deposition of matrix proteins in the myocardium. Myocardial fibrosis can be divided into “reactive interstitial” and “reparative” subtypes [2]. Reactive interstitial fibrosis is characterized by expansion of the myocardial interstitial space without significant loss of cardiomyocytes. Reparative fibrosis involves collagen deposition in response to myocardial ischemia. The adaptive responses to preserve cardiac output are reactive interstitial fibrosis and cardiomyocyte hypertrophy. Cardiomyocytes undergoing necrosis and apoptosis cause reparative fibrosis [3]. Myocardial fibrosis plays an important part in the pathogenesis of ischemic cardiomyopathy, which contributes to systolic and diastolic dysfunction. Ischemic injury to the heart leads to myocardial fibrosis, and the end result is heart failure
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