Journal
REDOX BIOLOGY
Volume 18, Issue -, Pages 211-221Publisher
ELSEVIER
DOI: 10.1016/j.redox.2018.07.007
Keywords
Melatonin; HFpEF; CTRP3; Adipocyte; Oxidative stress; Apoptosis
Categories
Funding
- National Natural Science Foundation of China [81600189, 81600191]
- Scientific and Technological Project of Henan Province [172102310531, 201403015]
- Education Department of Henan Province [16A320029]
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Melatonin has been shown to inhibit myocardial infarction-induced apoptosis, its function in heart failure with preserved ejection fraction (HFpEF) has not been investigated. This study aimed to investigate whether melatonin attenuates obesity-related HFpEF. Male mice were fed a high-fat diet (HFD) from weaning to 6 months of age to induce HFpEF. The mice were orally administered melatonin (50 mg/kg) by 3 weeks. Diastolic function was significantly improved by melatonin supplementation in mice fed an HFD. Melatonin attenuated obesity induced myocardial oxidative stress and apoptosis and promoted the secretion of C1q/tumour necrosis factor related protein 3 (CTRP3) by adipose tissue. And depletion of circulating CTRP3 largely abolished melatonin-mediated cardio-protection. Melatonin-mediated secretion of adipocyte-derived CTRP3 activated NF-E2-related factor 2 (Nrf2), which were largely abrogated by knocking down CTRP3 in adipocytes or Nrf2 in cardiomyocytes. Nrf2 activation was mediated by miR-200a, and a miR-200a antagomir offset the effects of melatonin-conditioned medium on Nrf2 expression. Our results indicate that melatonin can be used to treat and prevent obesity related HFpEF.
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