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.
Highlights
Myocardial hypertrophy includes physiological hypertrophy and pathological hypertrophy [1].Sustained pathologic myocardial hypertrophy may lead to congestive heart failure, arrhythmia, and sudden death
For Systolic blood pressure (SBP), diastolic blood pressure (DBP) and average mean artery pressure (MAP) measured by invasive artery catheterization, the two-way ANOVA indicated significant effects for transverse aortic constriction (TAC), but there were no marked effects for drug treatment or for TAC × drug treatment interaction
Post hoc analysis effects for TAC, but there were no marked effects for drug treatment or for TAC × drug treatment showed that there was no significant difference in SBP in mice of all the groups at the beginning of interaction
Summary
Myocardial hypertrophy includes physiological hypertrophy and pathological hypertrophy [1]. Sustained pathologic myocardial hypertrophy may lead to congestive heart failure, arrhythmia, and sudden death. It is one of the vital causes of many cardiovascular diseases [2]. The exact mechanism of myocardial hypertrophy has not been elucidated, which might be related to oxidative stress, energy metabolism, hemodynamic factors, neurohumoral factors, cardiovascular autocrine/paracrine regulation, insulin secretion, heredity, and so on [3,4,5,6]. Oxidative stress is the state that redox balance of the cell is broken, which means the reactive oxygen species (ROS) levels exceed the scavenging capacity.
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