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Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat

2018Journal article Open access
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dc.contributor.authorRocha, B.
dc.contributor.authorRodrigues, A. R.
dc.contributor.authorTomada, I.
dc.contributor.authorMartins, M. J.
dc.contributor.authorGuimarães, J. T.
dc.contributor.authorGouveia, A. M.
dc.contributor.authorAlmeida, H.
dc.contributor.authorNeves, D.
dc.date.accessioned2018-10-26T16:05:24Z
dc.date.available2018-10-26T16:05:24Z
dc.date.issued2018
dc.description.abstractBackground: Endothelial dysfunction underlies cardiovascular disease that frequently affects aged individuals. Characterized by local decrease in nitric oxide, it results from down-regulation of endothelial nitric oxide synthase (eNOS) expression/activity. Aiming to elucidate the molecular mechanisms involved in age-related endothelial dysfunction and to unveil potential therapeutic targets, we tested how diet pattern, exercise and atorvastatin modulate the expression of eNOS, inducible NOS (iNOS), endothelin-1, sirtuins (SIRT) and microRNA-155 in the erectile tissue of high-fat fed aged rats. Methods: Sprague-Dawley male rats fed with high-fat diet until they completed 12 months were grouped and subjected to energy restriction (ER), ER and atorvastatin, or, ER, atorvastatin and physical exercise. Controls were fed with standard rodent chow. The blood pressure was measured using the tail-cuff method before sacrifice at 18 months. Glucose, total cholesterol, HDL, triglyceride and CRP were assessed in blood and eNOS, endothelin-1, iNOS and sirtuins were detected by immunofluorescence in the penis sections; eNOS, endothelin-1, iNOS, SIRT2–4 and SIRT6–7 were semi-quantified by western blotting in tissue homogenates. MicroRNA-155 was quantified using RT-PCR in formalin-fixed paraffin embedded sections. To compare the studied variables, two-tail student t test was used. Results: Atorvastatin promotes eNOS expression and is more efficient than ER or exercise in the control of hyperlipidemia and inflammation. Among the studied sirtuins, detected for the first time in the erectile tissue of the aged rat, SIRT2 aligns with eNOS expression. Both proteins exhibit over-expression in animals with combined exercise, atorvastatin and ER. Analysis of microRNA-155 expression also suggests its intervention in the regulation of eNOS expression. ER, particularly when combined with atorvastatin, was able to reverse the increase of iNOS and endothelin-1 in high-fat fed rats. Conclusions: The present results indicate that the association of ER, atorvastatin and exercise is more efficient than isolated interventions in the prevention of endothelial dysfunction.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationRocha, B., Rodrigues, A.R., Tomada, I., Martins, M.J., Guimarães, J.T., Gouveia, A.M., … Neves, D. (2018). Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat. Nutrition & Metabolism, 15pt_PT
dc.identifier.doi10.1186/s12986-018-0265-zpt_PT
dc.identifier.eid85045506163
dc.identifier.issn1743-7075
dc.identifier.pmid29686722
dc.identifier.urihttp://hdl.handle.net/10400.14/25844
dc.identifier.wos000430211500001
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherBMCpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectEndothelial dysfunctionpt_PT
dc.subjectEnergy restrictionpt_PT
dc.subjectExercisept_PT
dc.subjectAtorvastatinpt_PT
dc.subjectSirtuinspt_PT
dc.subjectmicroRNA-155pt_PT
dc.titleEnergy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged ratpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBPD%2F92868%2F2013/PT
oaire.citation.titleNutrition and Metabolismpt_PT
oaire.citation.volume15
oaire.fundingStreamSFRH
person.familyNameRodrigues
person.familyNameTomada
person.familyNameMartins
person.familyNameGuimarães
person.familyNameGouveia
person.familyNameNeves
person.givenNameAdriana
person.givenNameInês
person.givenNameMaria João
person.givenNameJoão Tiago
person.givenNameAlexandra
person.givenNameDelminda
person.identifier2689332
person.identifierR-000-BVW
person.identifier.ciencia-id9A10-756A-D96A
person.identifier.ciencia-id7719-7A32-37A7
person.identifier.ciencia-id5413-5817-CE93
person.identifier.ciencia-idE817-6AD8-E6C3
person.identifier.ciencia-id2C15-98D1-4FA9
person.identifier.ciencia-id8C17-D9AB-804A
person.identifier.orcid0000-0002-9613-1552
person.identifier.orcid0000-0003-4660-0645
person.identifier.orcid0000-0002-3560-3261
person.identifier.orcid0000-0003-4836-6311
person.identifier.orcid0000-0001-8784-4246
person.identifier.orcid0000-0002-3301-8376
person.identifier.ridT-3079-2017
person.identifier.ridP-3525-2016
person.identifier.scopus-author-id25223739100
person.identifier.scopus-author-id25223994400
person.identifier.scopus-author-id7402262295
person.identifier.scopus-author-id7102733078
person.identifier.scopus-author-id7005609395
person.identifier.scopus-author-id8148778800
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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