Neuroprotection by post-stroke administration of an oral formulation of angiotensin-(1-7) in ischaemic stroke

dc.creatorDouglas M. Bennion
dc.creatorChad H. Jones
dc.creatorLauren L. Donnangelo
dc.creatorJustin T. Graham
dc.creatorJacob D. Isenberg
dc.creatorAlex N. Dang
dc.creatorVermali Rodriguez
dc.creatorRubén Dario Sinisterra Millán
dc.creatorFrederico Barros de Sousa
dc.creatorRobson Augusto Souza dos Santos
dc.creatorColin Sumners
dc.date.accessioned2023-12-11T15:47:39Z
dc.date.accessioned2025-09-09T01:09:07Z
dc.date.available2023-12-11T15:47:39Z
dc.date.issued2018
dc.description.sponsorshipOutra Agência
dc.identifier.doihttp://dx.doi.org/10.1113/EP086957
dc.identifier.issn1469-445X
dc.identifier.urihttps://hdl.handle.net/1843/61870
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofExperimental Physiology
dc.rightsAcesso Restrito
dc.subjectAngiotensina
dc.subjectEnzima conversora da angiotensina
dc.subjectFluxo sanguíneo
dc.subjectAcidentes vasculares cerebrais
dc.subjectCiclodextrinas
dc.subjectFisiologia experimental
dc.subject.otherAngiotensin-(1-7)
dc.subject.otherAngiotensin-converting enzyme 2
dc.subject.otherCerebral blood flow
dc.subject.otherIschaemic stroke
dc.subject.otherNeuroprotection
dc.titleNeuroprotection by post-stroke administration of an oral formulation of angiotensin-(1-7) in ischaemic stroke
dc.typeArtigo de periódico
local.citation.epage923
local.citation.issue6
local.citation.spage916
local.citation.volume103
local.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.
local.identifier.orcidhttps://orcid.org/0000-0003-3394-7164
local.identifier.orcidhttps://orcid.org/0000-0001-7656-1849
local.identifier.orcidhttps://orcid.org/0000-0002-7930-6867
local.identifier.orcidhttps://orcid.org/0000-0002-9689-2255
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.departmentICX - DEPARTAMENTO DE QUÍMICA
local.publisher.initialsUFMG
local.url.externahttps://physoc.onlinelibrary.wiley.com/doi/10.1113/EP086957

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