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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Autor*in:	Silvia Nistri [verfasserIn] Claudia Fiorillo [verfasserIn] Matteo Becatti [verfasserIn] Daniele Bani [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	relaxin serelaxin cardiac muscle cells ischemia-reperfusion hypoxia–reoxygenation oxidative stress

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 9(2020), 9, p 774
Übergeordnetes Werk:	volume:9 ; year:2020 ; number:9, p 774

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox9090774

Katalog-ID:	DOAJ063803402

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language	English
source	In Antioxidants 9(2020), 9, p 774 volume:9 year:2020 number:9, p 774
sourceStr	In Antioxidants 9(2020), 9, p 774 volume:9 year:2020 number:9, p 774
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institution	findex.gbv.de
topic_facet	relaxin serelaxin cardiac muscle cells ischemia-reperfusion hypoxia–reoxygenation oxidative stress Therapeutics. Pharmacology
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container_title	Antioxidants
authorswithroles_txt_mv	Silvia Nistri @@aut@@ Claudia Fiorillo @@aut@@ Matteo Becatti @@aut@@ Daniele Bani @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
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callnumber-first	R - Medicine
author	Silvia Nistri
spellingShingle	Silvia Nistri misc RM1-950 misc relaxin misc serelaxin misc cardiac muscle cells misc ischemia-reperfusion misc hypoxia–reoxygenation misc oxidative stress misc Therapeutics. Pharmacology 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
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topic_title	RM1-950 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 relaxin serelaxin cardiac muscle cells ischemia-reperfusion hypoxia–reoxygenation oxidative stress
topic	misc RM1-950 misc relaxin misc serelaxin misc cardiac muscle cells misc ischemia-reperfusion misc hypoxia–reoxygenation misc oxidative stress misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc relaxin misc serelaxin misc cardiac muscle cells misc ischemia-reperfusion misc hypoxia–reoxygenation misc oxidative stress misc Therapeutics. Pharmacology
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title	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
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title_full	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
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title_sort	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
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title_auth	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
abstract	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.
abstractGer	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.
abstract_unstemmed	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.
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title_short	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
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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

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