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      Melatonin protects against the pathological cardiac hypertrophy induced by transverse aortic constriction through activating PGC-1β: In vivo and in vitro studies.

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          Abstract

          Melatonin, a circadian molecule secreted by the pineal gland, confers a protective role against cardiac hypertrophy induced by hyperthyroidism, chronic hypoxia, and isoproterenol. However, its role against pressure overload-induced cardiac hypertrophy and the underlying mechanisms remains elusive. In this study, we investigated the pharmacological effects of melatonin on pathological cardiac hypertrophy induced by transverse aortic constriction (TAC). Male C57BL/6 mice underwent TAC or sham surgery at day 0 and were then treated with melatonin (20 mg/kg/day, via drinking water) for 4 or 8 weeks. The 8-week survival rate following TAC surgery was significantly increased by melatonin. Melatonin treatment for 8 weeks markedly ameliorated cardiac hypertrophy. Compared with the TAC group, melatonin treatment for both 4 and 8 weeks reduced pulmonary congestion, upregulated the expression level of α-myosin heavy chain, downregulated the expression level of β-myosin heavy chain and atrial natriuretic peptide, and attenuated the degree of cardiac fibrosis. In addition, melatonin treatment slowed the deterioration of cardiac contractile function caused by pressure overload. These effects of melatonin were accompanied by a significant upregulation in the expression of peroxisome proliferator-activated receptor-gamma co-activator-1 beta (PGC-1β) and the inhibition of oxidative stress. In vitro studies showed that melatonin also protects against angiotensin II-induced cardiomyocyte hypertrophy and oxidative stress, which were largely abolished by knocking down the expression of PGC-1β using small interfering RNA. In summary, our results demonstrate that melatonin protects against pathological cardiac hypertrophy induced by pressure overload through activating PGC-1β.

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          Author and article information

          Journal
          J. Pineal Res.
          Journal of pineal research
          Wiley
          1600-079X
          0742-3098
          Oct 2017
          : 63
          : 3
          Affiliations
          [1 ] Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
          [2 ] Cell Engineering Research Center and Department of Cell Biology, State Key Laboratory of Cancer, Fourth Military Medical University, Xi'an, China.
          [3 ] Institute of Material Medical, School of Pharmacy, Fourth Military Medical University, Xi'an, China.
          [4 ] The First Brigade of Student, Fourth Military Medical University, Xi'an, China.
          [5 ] Department of Biomedical Engineering, Fourth Military Medical University, Xi'an, China.
          [6 ] Department of Cellular and Structural Biology, UT Health Science Center, San Antonio, TX, USA.
          Article
          10.1111/jpi.12433
          28708271

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