Mostrar el registro sencillo del ítem

Artículo

dc.creatorMiguel Carrasco, José Luis
dc.creatorZambrano Sevilla, Sonia
dc.creatorBlanca Lobato, Antonio Jesús
dc.creatorMate Barrero, Alfonso
dc.creatorVázquez Cueto, Carmen María
dc.date.accessioned2015-09-23T10:02:50Z
dc.date.available2015-09-23T10:02:50Z
dc.date.issued2010
dc.identifier.issn1476-9255es
dc.identifier.urihttp://hdl.handle.net/11441/28738
dc.description.abstractBackground: Captopril is an angiotensin-converting enzyme (ACE) inhibitor widely used in the treatment of arterial hypertension and cardiovascular diseases. Our objective was to study whether captopril is able to attenuate the cardiac inflammatory process associated with arterial hypertension. Methods: Left ventricle mRNA expression and plasma levels of pro-inflammatory (interleukin-1β (IL-1β) and IL-6) and anti-inflammatory (IL-10) cytokines, were measured in spontaneously hypertensive rats (SHR) and their control normotensive, Wistar-Kyoto ( WKY ) rats, with or without a 12-week treatment with captopril (80 mg/Kg/day; n = six animals per group). To understand the mechanisms involved in the effect of captopril, mRNA expression of ACE, angiotensin II type I receptor (AT1R) and p22phox (a subu nit of NADPH oxidase), as well as NF-κB activation and expression, were measured in the left ventricle of these animals. Results: In SHR, the observed increases in blood pressures, heart rate, left ventricle relative weight, plasma levels and cardiac mRNA expression of IL-1β and IL-6, as well as the reductions in the plasma levels and in the cardiac mRNA expression of IL-10, were reversed afte r the treatment with captopril. Moreover, the mRNA expressions of ACE, AT1R and p22phox, which were enhanced in the left ventricle of SHR, were reduced to normal valu es after captopril treatment. Finally, SHR presented an elevated cardiac mRNA expression and activation of the transcription nuclear factor, NF-κB, accompanied by a reduced expression of its inhibitor, IκB; captopril administration corrected the observed changes in all these parameters. Conclusion: These findings show that captopril decreases the inflammation process in the left ventricle of hypertensive rats and suggest that NF-κB-driven inflammatory reactivity might be responsible for this effect through an inactivation of NF-κB-dependent pro-inflammatory factorses
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherBioMed Centrales
dc.relation.ispartofJournal of inflammation, 7, 21-29es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleCaptopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kBes
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessrightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Fisiologíaes
dc.relation.publisherversionhttp://dx.doi.org/10.1186/1476-9255-7-21es
dc.identifier.doihttp://dx.doi.org/10.1186/1476-9255-7-21es
dc.identifier.idushttps://idus.us.es/xmlui/handle/11441/28738

FicherosTamañoFormatoVerDescripción
1476-9255-7-21.pdf766.2KbIcon   [PDF] Ver/Abrir  

Este registro aparece en las siguientes colecciones

Mostrar el registro sencillo del ítem

Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Excepto si se señala otra cosa, la licencia del ítem se describe como: Attribution-NonCommercial-NoDerivatives 4.0 Internacional