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An in vivo model of ischemic stroke to study potential pharmacological targets

2023Conference object Open access
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dc.contributor.authorMendes, Priscila
dc.contributor.authorSolas, João
dc.contributor.authorSantos, Sofia
dc.contributor.authorFernandes, Adelaide
dc.contributor.authorRatilal, Bernardo
dc.contributor.authorMateus, Vanessa
dc.contributor.authorRocha, João
dc.date.accessioned2024-10-18T10:49:29Z
dc.date.available2024-10-18T10:49:29Z
dc.date.issued2023
dc.descriptionThis research was funded by Instituto Politécnico de Lisboa (IPL/2022/MCAO_ESTeSL) and Fundação para a Ciência e a Tecnologia (UIDB/05608/2020 and UIDP/05608/2020).pt_PT
dc.description.abstractBackground: Ischemic Stroke (IS) is caused by a focal disruption in cerebral blood flow due to the occlusion of a blood vessel, most commonly the middle cerebral artery (MCA)—the ischemic cascade results in neuronal death and inflammatory response, including in situ microglia activation. Inflammation is a double‐edged sword; it can cause tissue injury but can also help in the tissue repair of the brain. The only approved pharmacological treatment for IS has strong limitations of use depending on the time post-stroke onset. Despite the efforts to develop neuroprotective agents, none have proven efficacious for the human population. Aim: The aim is to clarify the cerebral cellular behavior during the different phases of ischemia-reperfusion as it might contribute to increasing pharmacological targets toward neuroprotection. Methods: The middle cerebral artery occlusion (MCAO) in vivo model was developed (n=8). Rats were randomly divided into two groups: 1) Animals exposed to 1h of ischemia (I1h) and 2) Animals exposed to 1h of ischemia followed by 1h of reperfusion (I/R1h). Brains were collected and the expression of synaptic markers (PSD-95, Syn), inflammatory mediators (TNF-α, IL-1β, IL-10), markers of microglia (Iba1, iNOS, Arg), and astrocytes (GFAP, S100B) were determined by qRealTime-PCR and Western Blot. Results: We found decreased PSD-95 and Syn expression in the ipsilateral hemisphere of both groups (~0.5 fold-I 1h; ~0.5 fold-I/R 1h), compared to the contralateral hemisphere. Levels of IL-10 were decreased in the ipsilateral hemisphere of both groups (~0.2 fold-I 1h; ~0.4 fold-I/R 1h), compared to the contralateral hemisphere. TNF-α was higher in the I/R 1h group compared to the I 1h group. Iba1 and GFAP expression were reduced in the ipsilateral hemisphere of the I/R 1h group (~0.4 fold and 0.8 fold, respectively). Conclusions: Our results strengthen the MCAO rodent model as a potential model to study neuroinflammation as a pharmacological target. Further research is needed to clarify time-dependent changes.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMendes P, Solas J, Santos S, Fernandes A, Ratilal B, Mateus V, et al. An in vivo model of ischemic stroke to study potential pharmacological targets. In: Proceedings of Research and Practice in Allied and Environmental Health – 11º Congresso Nacional da APLF. 2023;1(3):24.pt_PT
dc.identifier.doi10.26537/prpaeh.v1i3.5382pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.21/17754
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationIPL/2022/MCAO_ESTeSLpt_PT
dc.relation.publisherversionhttps://parc.ipp.pt/index.php/PRPAEH/article/view/5382pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectIschemiapt_PT
dc.subjectNeuroinflammationpt_PT
dc.subjectReperfusionpt_PT
dc.subjectStrokept_PT
dc.subjectIPL/2022/MCAO_ESTeSLpt_PT
dc.subjectUIDB/05608/2020pt_PT
dc.subjectUIDP/05608/2020pt_PT
dc.titleAn in vivo model of ischemic stroke to study potential pharmacological targetspt_PT
dc.typeconference object
dspace.entity.typePublication
oaire.citation.issue3pt_PT
oaire.citation.startPage24pt_PT
person.familyNameRodrigues Gomes Mendes
person.familyNamePinho Mateus
person.givenNamePriscila
person.givenNameVanessa Alexandra
person.identifier.ciencia-id6A16-5C18-F10B
person.identifier.ciencia-id5A12-571D-AD6A
person.identifier.orcid0000-0002-0013-3140
person.identifier.orcid0000-0002-3204-3772
rcaap.rightsopenAccesspt_PT
rcaap.typeconferenceObjectpt_PT
relation.isAuthorOfPublicationb02faa18-658e-4edc-b846-7c0b3646414c
relation.isAuthorOfPublication406041a5-682c-4f94-a4e2-ddbfc541313c
relation.isAuthorOfPublication.latestForDiscovery406041a5-682c-4f94-a4e2-ddbfc541313c

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