Abstract Title:

Puerarin suppresses Na+-K+-ATPase mediated systemic inflammation and CD36 expression, and alleviates cardiac lipotoxicity in vitro and in vivo.

Abstract Source:

J Cardiovasc Pharmacol. 2016 Sep 6. Epub 2016 Sep 6. PMID: 27606935

Abstract Author(s):

Hua Qin, Yan Zhang, Ru Wang, Xiaoyan Du, Liping Li, Haiwei Du

Article Affiliation:

Hua Qin

Abstract:

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 ELISA indicated that 15 μM puerarin treatment greatly increased Na-K-ATPase activity and decreased C-reactive protein (CRP) secretion, thus suppressing the expression of CD36, a key contributor to the FFA accumulation. Additionally, low dose puerarin (≤ 100 mg/Kg body weight) administration inproved 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 minitored on ex vivo working hearts which were obtained from WT, Tg control and Tg-puerarin mice. Compared with WT hearts, Tg hearts displayed a significantdecrease in Na/K-ATPase activity and glucose consumption rate, and a 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.

Study Type : Animal Study, In Vitro Study

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