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dc.contributor.authorMohammadi, S
dc.contributor.authorGarjani, A
dc.contributor.authorNajafi, M
dc.contributor.authorHamzeiy, H
dc.contributor.authorMaleki-Dizaji, N
dc.contributor.authorOmidi, Y
dc.contributor.authorFayezi, S
dc.contributor.authorDarabi, M
dc.contributor.authorMostafalou, S
dc.contributor.authorHassanzadeh, K
dc.contributor.authorKhani, S
dc.date.accessioned2018-08-26T08:04:30Z
dc.date.available2018-08-26T08:04:30Z
dc.date.issued2012
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/49582
dc.description.abstractMethylsulfonylmethane (MSM) is naturally accruing organic sulphur that is known as a potent anti-inflammatory compound. The aim of this study was to investigate the effect of MSM on mRNA expressions of angiotensinogen, endothelin-1 (ET-1) and Transforming Growth Factor (TGF)-beta 1 in rats with monocrotaline (MCT)-induced pulmonary arterial hypertension. Wistar rats were randomly assigned to 38-days pretreatment or 28-days treatment. MSM was administered to either 10 days before or 14 days after a single dose of MCT. Right Ventricle (RV) tissue samples were obtained to evaluate changes in the inflammatory genes expression using RT-PCR assay. The expression levels of angiotensinogen, ET-1 and TGF-beta 1 significantly were reduced (p<0.01) at efficient dose of MSM in MCT-induced pulmonary arterial hypertensive rats. Results suggest that harmful effects of MCT induced PAH on the RV function could be attenuated by anti-inflammatory actions through the suppression of local RAAS along with associated growth-promoting factors TGF-beta 1 and ET-1.
dc.language.isoEnglish
dc.relation.ispartofINTERNATIONAL JOURNAL OF PHARMACOLOGY
dc.subjectInflammation
dc.subjectright ventricle
dc.subjectmonocrotaline
dc.subjectendothelin-1
dc.subjectTGF-beta 1
dc.subjectangiotensinogen
dc.titleInhibitory Effects of Methylsulfonylmethane on Ventricular Hypertrophy Related Gene Expression
dc.typeArticle
dc.citation.volume8
dc.citation.issue7
dc.citation.spage647
dc.citation.epage651
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.3923/ijp.2012.647.651


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