Key result
Pretreatment with Biochanin-A for 30 days in rats with isoproterenol-induced myocardial infarction significantly reestablished altered lipid metabolism and suppressed proinflammatory cytokines and MMPs.
Why the study?
To assess the therapeutic potential of Biochanin-A pretreatment on lipid metabolic abnormalities, proinflammatory cytokines, and matrix metalloproteinase expression in isoproterenol-induced myocardial infarction in rats.
Does Biochanin-A pretreatment improve lipid metabolic abnormalities, proinflammatory cytokines, and matrix metalloproteinase expression in rats with isoproterenol-induced myocardial infarction?
Does Biochanin-A pretreatment improve lipid metabolic abnormalities, proinflammatory cytokines, and matrix metalloproteinase expression in rats with isoproterenol-induced myocardial infarction?
Answers are grounded in this paper and cite their sources.
Biochanin-A pretreatment attenuates lipid metabolic abnormalities, inflammation, and matrix metalloproteinase expression in a rat model of myocardial infarction, suggesting potential therapeutic value for heart failure.
In the present study, we assessed the therapeutic potential of Biochanin-A (BCA) (10 mg/kg BW/day) pretreatment for 30 days on lipid metabolic abnormalities, proinflammatory cytokines and matrix metalloproteinase expression in isoproterenol (ISO)-induced myocardial infarction (MI) in rats. We measured the potential role of BCA on tissue and circulatory lipid profiles as well as on lipid metabolic enzymes: serum inflammatory cytokines (TNF-α, IL-1α, IL-1β, IL-6 and MCP1) and serum Matrix Metalloproteinases (particularly, MMP-2 and MMP-9) together with mRNA expressions of TNF-α, IL-6, MMP-2 and MMP-9 by RT-PCR analysis. Administration of ISO to rats significantly distorted their lipid metabolism and augmented inflammatory process, MMP expression and proteolytic activity. In addition, pretreatment with BCA of ISO-induced MI rats significantly reestablished the altered lipid metabolism and concealed the inflammation of cytokines. BCA suppressed the expressions of proinflammatory cytokines and MMPs in ISO-induced MI in rats when compared to normal untreated MI rats. Hence, these results established that BCA could improve the pathological processes of myocardial remodeling which was confirmed by histopathology of heart in MI rats and might be an effective beneficial ingredient for the management of heart failure disorders.
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Govindasami et al. (2021) studied Isoproterenol-induced myocardial infarction. Biochanin-A (BCA) vs. Normal untreated MI rats was evaluated on Lipid metabolic abnormalities, proinflammatory cytokines, and matrix metalloproteinase expression. Pretreatment with Biochanin-A for 30 days in rats with isoproterenol-induced myocardial infarction significantly reestablished altered lipid metabolism and suppressed proinflammatory cytokines and MMPs.
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