Key result
Low-dose puerarin alleviates cardiac lipotoxicity and inflammation by suppressing Na-K-ATPase-mediated CD36 expression in mice.
Why the study?
The role of puerarin in the progression of lipotoxic cardiomyopathy and its effects on Na-K-ATPase activity, systemic inflammation, and CD36 expression were not fully understood.
Does puerarin alleviate cardiac lipotoxicity and systemic inflammation in a mouse model of lipotoxic cardiomyopathy?
Does puerarin alleviate cardiac lipotoxicity and systemic inflammation in a mouse model of lipotoxic cardiomyopathy?
Puerarin demonstrates protective effects against lipotoxic cardiomyopathy in preclinical models by modulating Na-K-ATPase activity and CD36 expression.
Does not support clinical use; leaves open translation of puerarin to human cardiac lipotoxicity.
Puerarin, a type of isoflavone, was shown to have multiple protective effects on myocardial injury. The objective of this study was to investigate the role of puerarin in the progression of lipotoxic cardiomyopathy. Primary cardiomyocytes were isolated from FATP1 transgenic (Tg) mice with lipotoxic cardiomyopathy, and various concentrations of puerarin were used to incubate with the cardiomyocytes. Our results showed low-dose puerarin (≤20 μM) treatment increased the cell viability and decreased the accumulation of free fatty acid (FFA). The data on enzyme-linked immunosorbent assay indicated that 15 μM puerarin treatment greatly increased Na-K-ATPase activity and decreased C-reactive protein secretion, thus suppressing the expression of CD36, a key contributor to the FFA accumulation. Additionally, low-dose puerarin (≤100 mg/kg body weight) administration improved Na-K-ATPase activity. Our data on serum analysis and histological detection in vivo indicated that systemic inflammation, CD36-induced lipid infiltration, and cardiomyocyte apoptosis were markedly alleviated in Tg mice injected with 90 mg/kg dose of puerarin. Finally, the uptake rates of H-palmitate and C-glucose were monitored on ex vivo working hearts that were obtained from wild-type (WT), Tg-control, and Tg-puerarin mice. Compared with WT hearts, Tg hearts displayed a significant decrease in Na/K-ATPase activity and glucose consumption rate and an increase in palmitate uptake rate and FFA accumulation. In Tg-puerarin hearts, Na/K-ATPase activity and glucose consumption rate were significantly rescued, and palmitate uptake and FFA accumulation were sharply suppressed. In conclusion, low-dose puerarin suppressed Na-K-ATPase-mediated CD36 expression and systemic inflammation and alleviated cardiac lipotoxicity in vitro and in vivo.
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Qin et al. (2016) studied Lipotoxic cardiomyopathy. Puerarin vs. Wild-type (WT) and Tg-control was evaluated on Na-K-ATPase activity, CD36 expression, systemic inflammation, and cardiac lipotoxicity. Low-dose puerarin suppressed Na-K-ATPase-mediated CD36 expression and systemic inflammation, and alleviated cardiac lipotoxicity in vitro and in vivo in a mouse model.
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