caa a22 4500 467934991 CHVBK 20180406152954.0 cr unu---uuuuu 170328e20061001xx s 000 0 eng 10.1007/s00408-005-2592-x doi (NATIONALLICENCE)springer-10.1007/s00408-005-2592-x Green Tea Extract Inhibits Paraquat-Induced Pulmonary Fibrosis by Suppression of Oxidative Stress and Endothelin-l Expression [Elektronische Daten] [Hak-Ryul Kim, Byung-Kyu Park, Yeon-Mok Oh, Yun-Song Lee, Dong-Soon Lee, Hyun-Kuk Kim, Joo-Young Kim, Tae-Sun Shim, Sang-Do Lee] 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 ETA 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. Springer Science+Business Media, Inc., 2006 Paraquat nationallicence Pulmonary fibrosis nationallicence Green tea extract nationallicence ET-1 nationallicence Oxidative stress nationallicence Kim Hak-Ryul Department of Internal Medicine, College of Medicine, Wonkwang University, Iksan, Republic of Korea aut Park Byung-Kyu Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut Oh Yeon-Mok Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, 388-1 Poongnab-dong, 138-736, Songpa-gu, Seoul, Republic of Korea aut Lee Yun-Song Department of Molecular and Cellular Biology, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea aut Lee Dong-Soon National Research Laboratory, Department of Laboratory Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea aut Kim Hyun-Kuk Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut Kim Joo-Young Asan Life Science Institute, Seoul, Republic of Korea aut Shim Tae-Sun Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut Lee Sang-Do Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut Lung Springer-Verlag; www.springer-ny.com 184/5(2006-10-01), 287-295 0341-2040 184:5<287 2006 184 408 https://doi.org/10.1007/s00408-005-2592-x text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00408-005-2592-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Kim Hak-Ryul Department of Internal Medicine, College of Medicine, Wonkwang University, Iksan, Republic of Korea aut NATIONALLICENCE 700 1- Park Byung-Kyu Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Oh Yeon-Mok Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, 388-1 Poongnab-dong, 138-736, Songpa-gu, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Lee Yun-Song Department of Molecular and Cellular Biology, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Lee Dong-Soon National Research Laboratory, Department of Laboratory Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Kim Hyun-Kuk Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Kim Joo-Young Asan Life Science Institute, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Shim Tae-Sun Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut NATIONALLICENCE 700 1- Lee Sang-Do Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Republic of Korea aut NATIONALLICENCE 773 0- Lung Springer-Verlag; www.springer-ny.com 184/5(2006-10-01), 287-295 0341-2040 184:5<287 2006 184 408 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer