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Int. J. Mol. Sci. 2018, 19(9), 2592; https://doi.org/10.3390/ijms19092592

Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement

1
Department of Pharmacology, School of Pharmacy and Key Laboratory of Inflammation and Molecular Drug Target of Jiangsu Province, Nantong University, Nantong 226001, China
2
School of Medicine, Nantong University, Nantong 226001, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 31 July 2018 / Revised: 28 August 2018 / Accepted: 29 August 2018 / Published: 31 August 2018
(This article belongs to the Special Issue Plant Natural Products for Human Health)
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Abstract

Dihydromyricetin (DMY), one of the flavonoids in vine tea, exerts several pharmacological actions. However, it is not clear whether DMY has a protective effect on pressure overload-induced myocardial hypertrophy. In the present study, male C57BL/6 mice aging 8–10 weeks were subjected to transverse aortic constriction (TAC) surgery after 2 weeks of DMY (250 mg/kg/day) intragastric administration. DMY was given for another 2 weeks after surgery. Blood pressure, myocardial structure, cardiomyocyte cross-sectional area, cardiac function, and cardiac index were observed. The level of oxidative stress in the myocardium was assessed with dihydroethidium staining. Our results showed that DMY had no significant effect on the blood pressure. DMY decreased inter ventricular septum and left ventricular posterior wall thickness, relative wall thickness, cardiomyocyte cross-sectional areas, as well as cardiac index after TAC. DMY pretreatment also significantly reduced arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP) mRNA and protein expressions, decreased reactive oxygen species production and malondialdehyde (MDA) level, while increased total antioxidant capacity (T-AOC), activity of superoxide dismutase (SOD), expression of sirtuin 3 (SIRT3), forkhead-box-protein 3a (FOXO3a) and SOD2, and SIRT3 activity in the myocardium of mice after TAC. Taken together, DMY ameliorated TAC induced myocardial hypertrophy in mice related to oxidative stress inhibition and SIRT3 pathway enhancement. View Full-Text
Keywords: dihydromyricetin; myocardial hypertrophy; oxidative stress; sirtuin 3 dihydromyricetin; myocardial hypertrophy; oxidative stress; sirtuin 3
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Chen, Y.; Luo, H.-Q.; Sun, L.-L.; Xu, M.-T.; Yu, J.; Liu, L.-L.; Zhang, J.-Y.; Wang, Y.-Q.; Wang, H.-X.; Bao, X.-F.; Meng, G.-L. Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement. Int. J. Mol. Sci. 2018, 19, 2592.

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