Please use this identifier to cite or link to this item: http://dspace.mediu.edu.my:8181/xmlui/handle/10261/2971
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dc.creatorSerrano-Mollar, Anna-
dc.creatorClosa, Daniel-
dc.creatorMorcillo, Esteban J.-
dc.creatorBulbena, Oriol-
dc.date2008-02-18T18:03:08Z-
dc.date2008-02-18T18:03:08Z-
dc.date2003-03-26-
dc.date.accessioned2017-01-31T01:00:10Z-
dc.date.available2017-01-31T01:00:10Z-
dc.identifierBritish Journal of Pharmacology 138(6): 1037–1048 (2003)-
dc.identifier0007-1188-
dc.identifierhttp://hdl.handle.net/10261/2971-
dc.identifier10.1038/sj.bjp.0705138-
dc.identifier.urihttp://dspace.mediu.edu.my:8181/xmlui/handle/10261/2971-
dc.descriptionThis 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.-
dc.descriptionThis 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).-
dc.descriptionPeer reviewed-
dc.format481474 bytes-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherWiley-Blackwell-
dc.relationhttp://dx.doi.org/10.1038/sj.bjp.0705138-
dc.rightsopenAccess-
dc.subjectPulmonary fibrosis-
dc.subjectBleomycin-
dc.subjectRat-
dc.subjectN-acetylcysteine-
dc.subjectInflammation-
dc.titleIn vivo antioxidant treatment protects against bleomycin-induced lung damage in rats-
dc.typeArtículo-
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