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首页> 中文期刊> 《老年心脏病学杂志》 >Small-molecule 7,8-dihydroxyflavone counteracts compensated and decompensated cardiac hypertrophy via AMPK activation

Small-molecule 7,8-dihydroxyflavone counteracts compensated and decompensated cardiac hypertrophy via AMPK activation

         
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BACKGROUND Pathological cardiac hypertrophy is a compensated response to various stimuli and is considered a key risk factor for heart failure.7,8-Dihydroxyflavone(7,8-DHF)is a flavonoid derivative that acts as a small-molecule brain-derived neurotrophic factor mimetic.The present study aimed to explore the potential role of 7,8-DHF in cardiac hypertrophy.METHODS Kunming mice and H9c2 cells were exposed to transverse aortic constriction or isoproterenol(ISO)with or without 7,8-DHF,respectively.F-actin staining was performed to calculate the cell area.Transcriptional levels of hypertrophic markers,including ANP,BNP,andβ-MHC,were detected.Echocardiography,hematoxylin-eosin staining,and transmission electron microscopy were used to examine the cardiac function,histology,and ultrastructure of ventricles.Protein levels of mitochondria-related factors,such as adenosine monophosphate-activated protein kinase(AMPK),and peroxisome proliferator-activated receptorγcoactivator-1α(PGC-1α),were detected.RESULTS 7,8-DHF inhibited compensated and decompensated cardiac hypertrophy,diminished the cross-sectional area,and alleviated the mitochondrial disorders of cardiomyocytes.Meanwhile,7,8-DHF reduced the cell size and repressed the mRNA levels of the hypertrophic markers of ISO-treated cardiomyocytes.In addition,7,8-DHF activated AMPK and PGC-1αsignals without affecting the protein levels of mitochondrial dynamics-related molecules.The effects of 7,8-DHF were eliminanted by Compound C,an AMPK inhibitor.CONCLUSIONS These findings suggest that 7,8-DHF inhibited cardiac hypertrophy and mitochondrial dysfunction by activating AMPK signaling,providing a potential agent for the treatment of pathological cardiac hypertrophy.

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