Human Relaxin-2 (Serelaxin) Attenuates Oxidative Stress in Cardiac Muscle Cells Exposed In Vitro to Hypoxia–Reoxygenation. Evidence for the Involvement of Reduced Glutathione Up-Regulation

Serelaxin (RLX) designates the pharmaceutical form of the human natural hormone relaxin-2 that has been shown to markedly reduce tissue and cell damage induced by hypoxia and reoxygenation (HR). The evidence that RLX exerts similar protective effects on different organs and cells at relatively low,...

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Bibliographic Details
Published in:Antioxidants 2020-09, Vol.9 (9), p.774
Main Authors: Nistri, Silvia, Fiorillo, Claudia, Becatti, Matteo, Bani, Daniele
Format: Article
Language:English
Subjects:
Antioxidants
Apoptosis
Cardiac muscle
cardiac muscle cells
Cobalt
Flow cytometry
Glutathione
Health aspects
Heart cells
Hypoxia
hypoxia–reoxygenation
ischemia-reperfusion
Lasers
Lipid peroxidation
Lipids
Metabolites
Microscopy
Mitochondria
Oxidative stress
Relaxin
serelaxin
Superoxide dismutase
Up-regulation
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Summary:Serelaxin (RLX) designates the pharmaceutical form of the human natural hormone relaxin-2 that has been shown to markedly reduce tissue and cell damage induced by hypoxia and reoxygenation (HR). The evidence that RLX exerts similar protective effects on different organs and cells at relatively low, nanomolar concentrations suggests that it specifically targets a common pathogenic mechanism of HR-induced damage, namely oxidative stress. In this study we offer experimental evidence that RLX (17 nmol L-1), added to the medium of HR-exposed H9c2 rat cardiac muscle cells, significantly reduces cell oxidative damage, mitochondrial dysfunction and apoptosis. These effects appear to rely on the up-regulation of the cellular availability of reduced glutathione (GSH), a ubiquitous endogenous antioxidant metabolite. Conversely, superoxide dismutase activity was not influenced by RLX, which, however, was not endowed with chemical antioxidant properties. Taken together, these findings verify the major pharmacological role of RLX in the protection against HR-induced oxidative stress, and shed first light on its mechanisms of action.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox9090774