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Vasonatrin peptide, a synthetic natriuretic peptide, attenuates myocardial injury and oxidative stress in isoprenaline-induced cardiomyocyte hypertrophy.

Authors
  • Chang, Pan1
  • Zhang, Xiaomeng2
  • Chen, Weiguo1
  • Zhang, Jing1
  • Wang, Jianbang1
  • Wang, Xihui1
  • Yu, Jun3
  • Zhu, Xiaoling4
  • 1 Department of Cardiology, the Second Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710038, China. , (China)
  • 2 Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China. , (China)
  • 3 Department of Cardiology, the Second Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710038, China; Clinical Experimental Center, Xi'an International Medical Center Hospital, Xi'an, Shaanxi 710100, China. Electronic address: [email protected] , (China)
  • 4 Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Peptides
Publication Date
Dec 24, 2020
Volume
137
Pages
170474–170474
Identifiers
DOI: 10.1016/j.peptides.2020.170474
PMID: 33359394
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Isoprenaline-induced cardiac hypertrophy can deteriorate to heart failure, which is a leading cause of mortality. Endogenous vasonatrin peptide (VNP) has been reported to be cardioprotective against myocardial ischemia/reperfusion injury in diabetic rats. However, little is known about the effect of exogenous VNP on cardiac hypertrophy. We further explored whether VNP attenuated isoprenaline-induced cardiomyocyte hypertrophy by examining the levels and activities of cGMP and PKG. In this study, we found that VNP significantly attenuated isoprenaline-induced myocardial hypertrophy and cardiac fibroblast activation in vivo. Moreover, VNP effectively halted the activation of apoptosis and oxidative stress in the isoprenaline-treated myocardium. VNP promoted superoxide dismutase (SOD) activity. Further study revealed that the protective effects of VNP might be mediated by the activity of the cGMP-PKG signaling pathway in vivo or in vitro, while the use of agonists and antagonists confirmed these results. Therefore, we demonstrated that the antiapoptosis and antioxidative stress effects of VNP depends on elevated cGMP-PKG signaling activity both in vivo and in vitro. These results suggest that VNP may be used in the treatment of myocardial hypertrophy. Copyright © 2020 Elsevier Inc. All rights reserved.

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