Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats

Abstract Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. Neutrophil infiltration and activation contributes to tissue damage, via the release of myeloperoxidase (MPO) and formation of the damaging oxidant hypo...

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Autores principales:	Luke Hall, Chaouri Guo, Sarah Tandy, Kathryn Broadhouse, Anthony C. Dona, Ernst Malle, Emil D. Bartels, Christina Christoffersen, Stuart M. Grieve, Gemma Figtree, Clare L. Hawkins, Michael J. Davies
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/24ee8bc94a0d461ab1c4070bbfe250ce
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spelling	oai:doaj.org-article:24ee8bc94a0d461ab1c4070bbfe250ce2021-12-02T17:24:09ZOral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats10.1038/s41598-021-92142-x2045-2322https://doaj.org/article/24ee8bc94a0d461ab1c4070bbfe250ce2021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92142-xhttps://doaj.org/toc/2045-2322Abstract Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. Neutrophil infiltration and activation contributes to tissue damage, via the release of myeloperoxidase (MPO) and formation of the damaging oxidant hypochlorous acid. We hypothesized that elevation of thiocyanate ions (SCN−), a competitive MPO substrate, would modulate tissue damage. Oral dosing of rats with SCN−, before acute ischemia–reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. No difference was observed in fractional shortening, but supplementation resulted in both left-ventricle end diastolic and left-ventricle end systolic areas returning to control levels, as determined by echocardiography. Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. SCN− supplementation did not modulate serum markers of damage/inflammation (ANP, BNP, galectin-3, CRP), but returned metabolomic abnormalities (reductions in histidine, creatine and leucine by 0.83-, 0.84- and 0.89-fold, respectively), determined by NMR, to control levels. These data indicate that elevated levels of the MPO substrate SCN−, which can be readily modulated by dietary means, can protect against acute ischemia–reperfusion injury.Luke HallChaouri GuoSarah TandyKathryn BroadhouseAnthony C. DonaErnst MalleEmil D. BartelsChristina ChristoffersenStuart M. GrieveGemma FigtreeClare L. HawkinsMichael J. DaviesNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-18 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Luke Hall Chaouri Guo Sarah Tandy Kathryn Broadhouse Anthony C. Dona Ernst Malle Emil D. Bartels Christina Christoffersen Stuart M. Grieve Gemma Figtree Clare L. Hawkins Michael J. Davies Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
description	Abstract Despite improvements in revascularization after a myocardial infarction, coronary disease remains a major contributor to global mortality. Neutrophil infiltration and activation contributes to tissue damage, via the release of myeloperoxidase (MPO) and formation of the damaging oxidant hypochlorous acid. We hypothesized that elevation of thiocyanate ions (SCN−), a competitive MPO substrate, would modulate tissue damage. Oral dosing of rats with SCN−, before acute ischemia–reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. No difference was observed in fractional shortening, but supplementation resulted in both left-ventricle end diastolic and left-ventricle end systolic areas returning to control levels, as determined by echocardiography. Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. SCN− supplementation did not modulate serum markers of damage/inflammation (ANP, BNP, galectin-3, CRP), but returned metabolomic abnormalities (reductions in histidine, creatine and leucine by 0.83-, 0.84- and 0.89-fold, respectively), determined by NMR, to control levels. These data indicate that elevated levels of the MPO substrate SCN−, which can be readily modulated by dietary means, can protect against acute ischemia–reperfusion injury.
format	article
author	Luke Hall Chaouri Guo Sarah Tandy Kathryn Broadhouse Anthony C. Dona Ernst Malle Emil D. Bartels Christina Christoffersen Stuart M. Grieve Gemma Figtree Clare L. Hawkins Michael J. Davies
author_facet	Luke Hall Chaouri Guo Sarah Tandy Kathryn Broadhouse Anthony C. Dona Ernst Malle Emil D. Bartels Christina Christoffersen Stuart M. Grieve Gemma Figtree Clare L. Hawkins Michael J. Davies
author_sort	Luke Hall
title	Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
title_short	Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
title_full	Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
title_fullStr	Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
title_full_unstemmed	Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats
title_sort	oral pre-treatment with thiocyanate (scn−) protects against myocardial ischaemia–reperfusion injury in rats
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/24ee8bc94a0d461ab1c4070bbfe250ce
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Oral pre-treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats

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