title: Sulforaphane improves oxidative status without attenuating the inflammatory response or cardiac impairment induced by ischemia-reperfusion in rats.
abstract: Sulforaphane, a natural isothiocyanate, demonstrates cardioprotection associated with its capacity to stimulate endogenous antioxidants and to inhibit inflammation. The aim of this study was to investigate whether sulforaphane is capable of attenuating oxidative stress and inflammatory responses through the TLR4/MyD88/NFκB pathway, and thereby could modulate post-ischemic ventricular function in isolated rat hearts submitted to ischemia and reperfusion. Male Wistar rats received sulforaphane (10 mg·kg(-1)·day(-1)) or vehicle i.p. for 3 days. Global ischemia was performed using isolated hearts, 24 h after the last injection, by interruption of the perfusion flow. The protocol included a 20 min pre-ischemic period followed by 20 min of ischemia and a 20 min reperfusion. Although no changes in mechanical function were observed, sulforaphane induced a significant increase in superoxide dismutase and heme oxygenase-1 expression (both 66%) and significantly reduced reactive oxygen species levels (7%). No differences were observed for catalase and glutathione peroxidase expression or their activities, nor for thioredoxin reductase, glutaredoxin reductase and glutathione-S-transferase. No differences were found in lipid peroxidation or TLR4, MyD88, and NF-κB expression. In conclusion, although sulforaphane was able to stimulate endogenous antioxidants modestly, this result did not impact inflammatory signaling or cardiac function of hearts submitted to ischemia and reperfusion.
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Jéssica Hellen Poletto
authors.initials: JH
authors.lastname: Bonetto
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Rafael Oliveira
authors.initials: RO
authors.lastname: Fernandes
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Bruna Gazzi de Lima
authors.initials: BG
authors.lastname: Seolin
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Dalvana Daneliza
authors.initials: DD
authors.lastname: Müller
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Rayane Brinck
authors.initials: RB
authors.lastname: Teixeira
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Alex Sander
authors.initials: AS
authors.lastname: Araujo
authors.affiliation: b Health Science Center of Vitória (EMESCAM), Espírito Santo, Brazil.
authors.forename: Dalton
authors.initials: D
authors.lastname: Vassallo
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Paulo Cavalheiro
authors.initials: PC
authors.lastname: Schenkel
authors.affiliation: a Laboratory of Cardiovascular Physiology, Institute of Basic Health Science (ICBS), Federal University of Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil.
authors.forename: Adriane
authors.initials: A
authors.lastname: Belló-Klein
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D002316:Cardiotonic Agents / Q000627:therapeutic use; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D051547:Heme Oxygenase-1 / Q000737:chemistry / Q000378:metabolism; D066298:In Vitro Techniques; D017879:Isothiocyanates / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D016328:NF-kappa B; D018384:Oxidative Stress / Q000187:drug effects*; D010477:Perfusion; D011897:Random Allocation; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013454:Sulfoxides; D013482:Superoxide Dismutase / Q000737:chemistry / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D002316:Cardiotonic Agents; D017879:Isothiocyanates; C507781:Myd88 protein, rat; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D013454:Sulfoxides; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase; C016766:sulforaphane
keywords: TLR4; cœur isolé; dérivés réactifs de l’oxygène; inflammation; ischemia–reperfusion; ischémie–reperfusion; isolated heart; oxidative stress; reactive oxygen species; stress oxydatif; sulforaphane