期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 19, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/ijms19092592
关键词
dihydromyricetin; myocardial hypertrophy; oxidative stress; sirtuin 3
资金
- National Natural Science Foundation of China [81770279, 31500649]
- Natural Science Research in Jiangsu Higher Education Institutions [18KJA310005]
- China Postdoctoral Science Foundation [2017M610342]
- Postgraduate Research & Practice Innovation Program of Jiangsu Province [1701050A]
- Research and Innovation Project of Graduate Students in Jiangsu Province [KYCX18_2401]
- Natural Science Foundation of Nantong City [MS12015015, MS12015101]
- Nantong University Cooperative Innovation Program of Small Molecular Compound RD [NTU2016-1]
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.
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