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dc.contributor.authorFracasso, Bianca de Moraespt_BR
dc.contributor.authorRangel, Juliana Oliveirapt_BR
dc.contributor.authorMachado, Alessandra Gonçalvespt_BR
dc.contributor.authorCuruja, Fernanda Severopt_BR
dc.contributor.authorLopes, Amandapt_BR
dc.contributor.authorOlsen, Virgílio da Rochapt_BR
dc.contributor.authorClausell, Nadine Oliveirapt_BR
dc.contributor.authorBiolo, Andreiapt_BR
dc.contributor.authorRohde, Luis Eduardo Paimpt_BR
dc.contributor.authorAndrades, Michael Evertonpt_BR
dc.date.accessioned2020-11-14T04:23:09Zpt_BR
dc.date.issued2019pt_BR
dc.identifier.issn1932-6203pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/215046pt_BR
dc.description.abstractCirculating advanced glycation end products (AGE) and their receptor, RAGE, are increased after a myocardial infarction (MI) episode and seem to be associated with worse prognosis in patients. Despite the increasing importance of these molecules in the course of cardiac diseases, they have never been characterized in an animal model of MI. Thus, the aim of this study was to characterize AGE formation and RAGE expression in plasma and cardiac tissue during cardiac remodeling after MI in rats. Adult male Wistar rats were randomized to receive sham surgery (n = 15) or MI induction (n = 14) by left anterior descending coronary artery ligation. The MI group was stratified into two subgroups based on postoperative left ventricular ejection fraction: low (MIlowEF) and intermediate (MIintermEF). Echocardiography findings and plasma levels of AGEs, protein carbonyl, and free amines were assessed at baseline and 2, 30, and 120 days postoperatively. At the end of follow-up, the heart was harvested for AGE and RAGE evaluation. No differences were observed in AGE formation in plasma, except for a decrease in absorbance in MIlowEF at the end of follow-up. A decrease in yellowish-brown AGEs in heart homogenate was found, which was confirmed by immunodetection of N-ε-carboxymethyl-lysine. No differences could be seen in plasma RAGE levels among the groups, despite an increase in MI groups over the time. However, MI animals presented an increase of 50% in heart RAGE at the end of the follow-up. Despite the inflammatory and oxidative profile of experimental MI in rats, there was no increase in plasma AGE or RAGE levels. However, AGE levels in cardiac tissue declined. Thus, we suggest that the rat MI model should be employed with caution when studying the AGERAGE signaling axis or anti-AGE drugs for not reflecting previous clinical findings.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofPloS one. San Francisco. Vol. 14, no. 1 (2019), e0209964, 16 p.pt_BR
dc.rightsOpen Accessen
dc.subjectReceptor para produtos finais de glicação avançadapt_BR
dc.subjectInfarto do miocárdiopt_BR
dc.subjectModelos animaispt_BR
dc.titleCharacterization of advanced glycation end products and their receptor (RAGE) in an animal model of myocardial infarctionpt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001117876pt_BR
dc.type.originEstrangeiropt_BR


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