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Green tea extract inhibits paraquat-induced pulmonary fibrosis by suppression of oxidative stress and endothelin-l expression

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dc.contributor.authorKim, Hak-Ryul-
dc.contributor.authorPark, Byung-Kyu-
dc.contributor.authorOh, Yeon-Mok-
dc.contributor.authorLee, Yun-Song-
dc.contributor.authorLee, Dong-Soon-
dc.contributor.authorKim, Hyun-Kuk-
dc.contributor.authorKim, Joo-Young-
dc.contributor.authorShim, Tae-Sun-
dc.contributor.authorLee, Sang-Do-
dc.date.accessioned2009-11-10T14:44:17Z-
dc.date.available2009-11-10T14:44:17Z-
dc.date.issued2006-
dc.identifier.citationLung 184:287-295en
dc.identifier.issn0341-2040 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17235729-
dc.identifier.urihttp://hdl.handle.net/10371/11871-
dc.description.abstractParaquat-induced pulmonary fibrosis involves two factors, direct injury by oxygen free radicals and indirect injury by inflammatory cells and fibroblasts. Endothelin-1 (ET-1) has been shown to act as a mediator of pulmonary fibrosis, and its formation increases during oxidative stress. We investigated whether green tea extract (GTE), which has antioxidant properties, inhibits paraquat-induced pulmonary fibrosis and whether ET-1 is involved in this process. Paraquat (0.3 mg/kg) was instilled into the right lungs of rats, following which the rats were either not further treated (Group P, n = 7), or they were administered 1% GTE mixed with feed (Group PG; n = 7) or the ET(A) receptor antagonist ZD2574 (10 mg/kg through gavage; Group PZ; n = 7) for two weeks. As control, we used rats instilled with saline (Group N; n = 6). Two weeks after paraquat instillation, we assayed the degree of pulmonary fibrosis by light microscopic morphometry and hydroxyproline content; lipid peroxidation as a marker of oxidative stresses by measurement of malondialdehyde (MDA); ET-1 by immunohistochemistry; and prepro-ET-1 mRNA expression by reverse transcription-polymerase chain reaction. Compared with Group N, significant pulmonary fibrosis was observed in Group P, accompanied by increases in MDA, ET-1, and prepro-ET-1 mRNA expression. Compared with Group P, Group PG showed significant decreases in pulmonary fibrosis, along with decreases in MDA, ET-1, and prepro-ET-1 mRNA expression. We also observed significant decreases in pulmonary fibrosis in Group PZ compared with Group P. These findings suggest that GTE inhibits paraquat-induced pulmonary fibrosis by suppression of oxidative stress and ET-1 expression.en
dc.language.isoenen
dc.publisherSpringer Verlagen
dc.subjectCamellia sinensisen
dc.subjectDisease Models, Animalen
dc.subjectEndothelin-1/biosynthesis/*geneticsen
dc.subjectGene Expression/*drug effectsen
dc.subjectHerbicides/toxicityen
dc.subjectImmunohistochemistryen
dc.subjectMalondialdehyde/metabolismen
dc.subjectOxidative Stress/*drug effectsen
dc.subjectParaquat/toxicityen
dc.subjectPlant Extracts/*therapeutic useen
dc.subjectPulmonary Fibrosis/chemically induced/*drug therapy/metabolismen
dc.subjectRNA/*geneticsen
dc.subjectRats, Sprague-Dawleyen
dc.subjectReverse Transcriptase Polymerase Chain Reactionen
dc.subjectTreatment Outcomeen
dc.titleGreen tea extract inhibits paraquat-induced pulmonary fibrosis by suppression of oxidative stress and endothelin-l expressionen
dc.typeArticleen
dc.contributor.AlternativeAuthor김학렬-
dc.contributor.AlternativeAuthor박병규-
dc.contributor.AlternativeAuthor오연목-
dc.contributor.AlternativeAuthor이윤송-
dc.contributor.AlternativeAuthor이동순-
dc.contributor.AlternativeAuthor김현국-
dc.contributor.AlternativeAuthor김주영-
dc.contributor.AlternativeAuthor심태선-
dc.contributor.AlternativeAuthor이상도-
dc.identifier.doi10.1007/s00408-005-2592-x-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Laboratory Medicine (검사의학전공)Journal Papers (저널논문_검사의학전공)
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