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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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Authors
Kim, Hak-Ryul; Park, Byung-Kyu; Oh, Yeon-Mok; Lee, Yun-Song; Lee, Dong-Soon; Kim, Hyun-Kuk; Kim, Joo-Young; Shim, Tae-Sun; Lee, Sang-Do
Issue Date
2006
Publisher
Springer Verlag
Citation
Lung 184:287-295
Keywords
Camellia sinensisDisease Models, AnimalEndothelin-1/biosynthesis/*geneticsGene Expression/*drug effectsHerbicides/toxicityImmunohistochemistryMalondialdehyde/metabolismOxidative Stress/*drug effectsParaquat/toxicityPlant Extracts/*therapeutic usePulmonary Fibrosis/chemically induced/*drug therapy/metabolismRNA/*geneticsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionTreatment Outcome
Abstract
Paraquat-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.
ISSN
0341-2040 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17235729

http://hdl.handle.net/10371/11871
DOI
https://doi.org/10.1007/s00408-005-2592-x
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College of Medicine/School of Medicine (의과대학/대학원)Laboratory Medicine (검사의학전공)Journal Papers (저널논문_검사의학전공)
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