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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/61870
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dc.creatorDouglas M. Bennionpt_BR
dc.creatorChad H. Jonespt_BR
dc.creatorLauren L. Donnangelopt_BR
dc.creatorJustin T. Grahampt_BR
dc.creatorJacob D. Isenbergpt_BR
dc.creatorAlex N. Dangpt_BR
dc.creatorVermali Rodriguezpt_BR
dc.creatorRubén Dario Sinisterra Millánpt_BR
dc.creatorFrederico Barros de Sousapt_BR
dc.creatorRobson Augusto Souza dos Santospt_BR
dc.creatorColin Sumnerspt_BR
dc.date.accessioned2023-12-11T15:47:39Z-
dc.date.available2023-12-11T15:47:39Z-
dc.date.issued2018-
dc.citation.volume103pt_BR
dc.citation.issue6pt_BR
dc.citation.spage916pt_BR
dc.citation.epage923pt_BR
dc.identifier.doihttp://dx.doi.org/10.1113/EP086957pt_BR
dc.identifier.issn1469-445Xpt_BR
dc.identifier.urihttp://hdl.handle.net/1843/61870-
dc.description.resumoAs a target for stroke therapies, the angiotensin-converting enzyme 2–angiotensin-(1–7)–Mas [ACE2/Ang-(1–7)/Mas] axis of the renin–angiotensin system can be activated chronically to induce neuroprotective effects, in opposition to the deleterious effects of angiotensin II via its type 1 receptor. However, more clinically relevant treatment protocols with Ang-(1–7) that involve its systemic administration beginning after the onset of ischaemia have not been tested. In this study, we tested systemic post-stroke treatments using a molecule where Ang-(1–7) is included within hydroxypropyl-𝛽-cyclodextrin [HP𝛽CD–Ang-(1–7)] as an orally bioavailable treatment. In three separate protocols, HP𝛽CD–Ang-(1–7) was administered orally to Sprague–Dawley rats after induction of ischaemic stroke by endothelin-1-induced middle cerebral artery occlusion: (i) to assess its effects on cerebral damage and behavioural deficits; (ii) to determine its effects on cardiovascular parameters; and (iii) to determine whether it altered cerebral blood flow. The results indicate that post-stroke oral administration of HP𝛽CD–Ang-(1–7) resulted in 25% reductions in cerebral infarct volumes and improvement in neurological functions (P < 0.05), without inducing any alterations in blood pressure, heart rate or cerebral blood flow. In conclusion, Ang-(1–7) treatment using an oral formulation after the onset of ischaemia induces significant neuroprotection in stroke and might represent a viable approach for taking advantage of the protective ACE2/Ang-(1–7)/Mas axis in this disease.pt_BR
dc.description.sponsorshipOutra Agênciapt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICX - DEPARTAMENTO DE QUÍMICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofExperimental Physiologypt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectAngiotensin-(1-7)pt_BR
dc.subjectAngiotensin-converting enzyme 2pt_BR
dc.subjectCerebral blood flowpt_BR
dc.subjectIschaemic strokept_BR
dc.subjectNeuroprotectionpt_BR
dc.subject.otherAngiotensinapt_BR
dc.subject.otherEnzima conversora da angiotensinapt_BR
dc.subject.otherFluxo sanguíneopt_BR
dc.subject.otherAcidentes vasculares cerebraispt_BR
dc.subject.otherCiclodextrinaspt_BR
dc.subject.otherFisiologia experimentalpt_BR
dc.titleNeuroprotection by post-stroke administration of an oral formulation of angiotensin-(1-7) in ischaemic strokept_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://physoc.onlinelibrary.wiley.com/doi/10.1113/EP086957pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3394-7164pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7656-1849pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7930-6867pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9689-2255pt_BR
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