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dc.contributor.authorSerrano-Mollar, Anna-
dc.contributor.authorClosa, Daniel-
dc.contributor.authorMorcillo, Esteban J.-
dc.contributor.authorBulbena, Oriol-
dc.date.accessioned2008-02-18T18:03:08Z-
dc.date.available2008-02-18T18:03:08Z-
dc.date.issued2003-03-26-
dc.identifier.citationBritish Journal of Pharmacology 138(6): 1037–1048 (2003)en_US
dc.identifier.issn0007-1188-
dc.identifier.urihttp://hdl.handle.net/10261/2971-
dc.description.abstractThis study examines the activity of the antioxidant N-acetylcysteine on bleomycin-induced pulmonary fibrosis in rats with emphasis on the early inflammatory phase. Rats receiving N-acetylcysteine (300 mg kg−1 day−1, intraperitoneal) had less augmented lung wet weight, and lower levels of proteins, lactate dehydrogenase, neutrophil and macrophage counts in bronchoalveolar lavage fluid and lung myeloperoxidase activity with a betterment of histological score at 3 days postbleomycin. A diminished lung GSH/GSSG ratio and augmented lipid hydroperoxides were observed 3 days postbleomycin. These changes were attenuated by N-acetylcysteine. Alveolar macrophages from bleomycin-exposed rats released augmented amounts of superoxide anion and nitric oxide. N-Acetylcysteine did not modify superoxide anion generation but reduced the increased production of nitric oxide. N-Acetylcysteine suppressed the bleomycin-induced increased activation of lung NF-κB (shift assay and immunohistochemistry), and decreased the augmented levels of the early inflammatory cytokines, tumour necrosis factor-α, interleukin-β, interleukin-6 and macrophage inflammatory protein-2 observed in bronchoalveolar lavage fluid at 1 and 3 days postbleomycin exposure. At 15 days postbleomycin, N-acetylcysteine decreased collagen deposition in bleomycin-exposed rats (hydroxyproline content: 6351±669 and 4626±288 μg per lung in drug vehicle- and N-acetylcysteine-treated rats, respectively; P<0.05). Semiquantitative histological assessment at this stage showed less collagen deposition in N-acetylcysteine-treated rats compared to those receiving bleomycin alone. These results indicate that N-acetylcysteine reduces the primary inflammatory events, thus preventing cellular damage and the subsequent development of pulmonary fibrosis in the bleomycin rat model.en_US
dc.description.sponsorshipThis work was supported by Grant 1FD97-1143 from the European Union (Regional Development Funds, FEDER), CICYT (Spanish Government), Regional Government (Generalitat Valenciana) and Grant FIS98/1367 (Spanish Ministry of Health).en_US
dc.format.extent481474 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherWiley-Blackwellen_US
dc.rightsopenAccessen_US
dc.subjectPulmonary fibrosisen_US
dc.subjectBleomycinen_US
dc.subjectRaten_US
dc.subjectN-acetylcysteineen_US
dc.subjectInflammationen_US
dc.titleIn vivo antioxidant treatment protects against bleomycin-induced lung damage in ratsen_US
dc.typeartículoen_US
dc.identifier.doi10.1038/sj.bjp.0705138-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1038/sj.bjp.0705138-
dc.identifier.pmid12684259-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.fulltextWith Fulltext-
item.openairetypeartículo-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.languageiso639-1en-
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