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dc.contributor.authorRobles-Vera, Iñaki
dc.contributor.authorde la Visitación, Néstor
dc.contributor.authorSánchez, Manuel
dc.contributor.authorGómez-Guzmán, Manuel
dc.contributor.authorJiménez, Rosario
dc.contributor.authorMoleón, Javier
dc.contributor.authorGonzález-Correa, Cristina
dc.contributor.authorRomero, Miguel
dc.contributor.authorYang, Tao
dc.contributor.authorRaizada, Mohan K
dc.contributor.authorToral, Marta 
dc.contributor.authorDuarte, Juan
dc.date.accessioned2021-05-07T09:45:44Z
dc.date.available2021-05-07T09:45:44Z
dc.date.issued2020-11-28
dc.identifier.citationAntioxidants (Basel). 2020; 9(12):e1199es_ES
dc.identifier.issn2076-3921es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12897
dc.description.abstractMicrobiota is involved in the host blood pressure (BP) regulation. The immunosuppressive drug mofetil mycophenolate (MMF) ameliorates hypertension. The present study analyzed whether MMF improves dysbiosis in mineralocorticoid-induced hypertension. Male Wistar rats were assigned to three groups: untreated (CTR), deoxycorticosterone acetate (DOCA)-salt, and DOCA treated with MMF for 4 weeks. MMF treatment reduced systolic BP, improved endothelial dysfunction, and reduced oxidative stress and inflammation in aorta. A clear separation in the gut bacterial community between CTR and DOCA groups was found, whereas the cluster belonging to DOCA-MMF group was found to be intermixed. No changes were found at the phylum level among all experimental groups. MMF restored the elevation in lactate-producing bacteria found in DOCA-salt joined to an increase in the acetate-producing bacteria. MMF restored the percentage of anaerobic bacteria in the DOCA-salt group to values similar to control rats. The improvement of gut dysbiosis was associated with an enhanced colonic integrity and a decreased sympathetic drive in the gut. MMF inhibited neuroinflammation in the paraventricular nuclei in the hypothalamus. This study demonstrates for the first time that MMF reduces gut dysbiosis in DOCA-salt hypertension models. This effect seems to be related to its capacity to improve gut integrity due to reduced sympathetic drive in the gut associated with reduced brain neuroinflammation.es_ES
dc.description.sponsorshipThis work was supported by Grants from Comisión Interministerial de Ciencia y Tecnología, Ministerio de Economía y competitividad (SAF2017-84894-R), Junta de Andalucía (CTS-164), with funds from the European Union, Ministerio de Economia y Competitividad, Instituto de Salud Carlos III (CIBER-CV), Spain, and National Heart, Lung and Blood Institute (NHLBI) grant HL102033. M.T. is a postdoctoral fellow of Instituto de Salud Carlos III (Sara Borrell Program). I.R.V. is a predoctoral fellow of MINECO. The cost of this publication was paid in part with funds from the European Union (Fondo Europeo de Desarrollo Regional, FEDER, “FEDER una manera de hacer Europa”).es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleMycophenolate Improves Brain-Gut Axis Inducing Remodeling of Gut Microbiota in DOCA-Salt Hypertensive Rats.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33260593es_ES
dc.format.volume9es_ES
dc.format.number12es_ES
dc.identifier.doi10.3390/antiox9121199es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderRegional Government of Andalusia (España) 
dc.contributor.funderUnión Europea 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderNIH - National Heart, Lung, and Blood Institute (NHLBI) (Estados Unidos) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/antiox9121199es_ES
dc.identifier.journalAntioxidants (Basel, Switzerland)es_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regulación Génica en Remodelado Vascular e Inflamaciónes_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2017-84894-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CTS-164es_ES
dc.rights.accessRightsopen accesses_ES


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