Key result
Ginsenoside Re (135 mg/kg daily for 4 weeks) improved cardiac function, prevented left ventricular dilatation, and decreased interstitial fibrosis in a rat model of myocardial infarction.
Why the study?
Ginsenoside Re protects against cardiovascular diseases, but its protective effects and mechanisms on cardiac function and left ventricular remodeling after myocardial infarction required investigation.
Does Ginsenoside Re improve cardiac function and mitigate ventricular remodeling in a rat model of myocardial infarction?
Does Ginsenoside Re improve cardiac function and mitigate ventricular remodeling in a rat model of myocardial infarction?
Ginsenoside Re preserves cardiac function and ameliorates left ventricular remodeling in a rat model of myocardial infarction, potentially through AMPK/TGF-β1/Smad2/3 and FAK/PI3K p110α/Akt signaling pathways.
Should not yet change post-MI management; leaves open translational studies of Ginsenoside Re for ventricular remodeling.
Ginsenoside Re, an herbal ingredient from ginseng, has been demonstrated to protect the heart from various cardiovascular diseases. In this study, we investigated the protective effects and mechanisms of ginsenoside Re (Gin-Re) on cardiac function and left ventricular remodeling in a rat model of myocardial infarction (MI). After ligating the left anterior descending coronary artery, Wistar rats were treated with Gin-Re (135 mg/kg) by gavage everyday for 4 weeks. Serological detection showed that Gin-Re significantly inhibited myocardial injury and attenuated oxidative stress in MI rats. Echocardiographic observation showed that Gin-Re significantly improved cardiac function and prevented left ventricular dilatation induced by MI. Pathological observation found that Gin-Re significantly decreased interstitial fibrosis in the left ventricle of MI rats. Compared with the MI group, Gin-Re treatment promoted AMPKα phosphorylation, decreased TGF-β1 expression, and attenuated Smad2/3 activation. After Gin-Re treatment, the phosphorylation of FAK, PI3K p110α, and Akt was enhanced in MI rats, while PI3K p110β showed no difference compared with the MI group. These results indicate that Gin-Re may improve MI-induced cardiac dysfunction and mitigate ventricular remodeling through regulation of the AMPK/TGF-β1/Smad2/3 and FAK/PI3K p110α/Akt signaling pathways.
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Yu et al. (2019) studied Myocardial Infarction. Ginsenoside Re vs. MI group was evaluated on Cardiac function and left ventricular remodeling. Ginsenoside Re (135 mg/kg daily for 4 weeks) improved cardiac function, prevented left ventricular dilatation, and decreased interstitial fibrosis in a rat model of myocardial infarction.
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