The anti-fibrotic effect of green tea with a high catechin content in the galactosamine-injured rat liver

被引:12
作者
Abe, Kouichi
Suzuki, Takuji
Ijiri, Mitsuhiro
Koyama, Yu
Isemura, Mamoru [1 ]
Kinae, Naohide
机构
[1] Univ Shizuoka, Grad Sch Nutr & Environm Sci, Shizuoka 4228526, Japan
[2] Univ Shizuoka, COE Century 21st, Shizuoka 4228526, Japan
[3] Kumiai Chem Ind Co Ltd, Shizuoka 4390031, Japan
[4] Hamamatsu Univ Sch Med, Dept Hlth Nutr, Hamamatsu, Shizuoka, Japan
来源
BIOMEDICAL RESEARCH-TOKYO | 2007年 / 28卷 / 01期
关键词
D O I
10.2220/biomedres.28.43
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Previously, we reported that the oral administration of green tea rich in catechins restored levels of several biomarkers increasing in gal actosamine-treated rats to nearly control values. These biomarkers included serum transaminase activities, serum concentrations of tumor necrosis factor-a and interleukin I-beta, and the hepatic mRNA expression of these inflammatory cytokines. In the present study, we examined possible anti-fibrotic effects of green tea in galactosamine-induced hepatitis. The results of the reverse transcription and polymerase chain reaction indicated that the increase in gene expression of the alpha 1 chain of collagen type 1 and transforming growth factor beta-1 in the injured liver 24 h post-injection of galactosamine was suppressed by the administration of green tea. Masson's trichrome staining demonstrated that the extent of fibrogenesis after 14 days was greater in the galactosamine-injured livers not treated with green tea than the treated ones. These results suggest that the drinking of green tea with a high catechin content may help to prevent and/or attenuate the development of fibrosis in hepatitis.
引用
收藏
页码:43 / 48
页数:6
相关论文
共 22 条
[1]   Green tea with a high catechin content suppresses inflammatory cytokine expression in the galactosamine-injured rat liver [J].
Abe, Kouichi ;
Ijiri, Mitsuhiro ;
Suzuki, Takuji ;
Taguchi, Kyoko ;
Koyama, Yu ;
Isemura, Mamoru .
BIOMEDICAL RESEARCH-TOKYO, 2005, 26 (05) :187-192
[2]   TRANSFORMING GROWTH FACTOR-BETA-1 AND FACTOR-ALPHA IN CHRONIC LIVER-DISEASE - EFFECTS OF INTERFERON ALFA THERAPY [J].
CASTILLA, A ;
PRIETO, J ;
FAUSTO, N .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 324 (14) :933-940
[3]   Expression of Tumor Necrosis Factor-alpha and Transforming Growth Factor-beta in Acute Liver Injury [J].
Czaja, Mark J. ;
Flanders, Kathleen C. ;
Biempica, Luis ;
Klein, Charna ;
Zern, Mark A. ;
Weiner, Francis R. .
GROWTH FACTORS, 1989, 1 (03) :219-226
[4]   INVITRO AND INVIVO ASSOCIATION OF TRANSFORMING GROWTH FACTOR-BETA-1 WITH HEPATIC-FIBROSIS [J].
CZAJA, MJ ;
WEINER, FR ;
FLANDERS, KC ;
GIAMBRONE, MA ;
WIND, R ;
BIEMPICA, L ;
ZERN, MA .
JOURNAL OF CELL BIOLOGY, 1989, 108 (06) :2477-2482
[5]   Modulation of transforming growth factor β function in hepatocytes and hepatic stellate cells in rat liver injury [J].
Date, M ;
Matsuzaki, K ;
Matsushita, M ;
Tahashi, Y ;
Furukawa, F ;
Inoue, K .
GUT, 2000, 46 (05) :719-724
[6]  
FRIEDMAN SL, 1993, NEW ENGL J MED, V328, P1828
[7]   Roles of TGF-beta in hepatic fibrosis [J].
Gressner, AM ;
Weiskirchen, R ;
Breitkopf, K ;
Dooley, S .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2002, 7 :D793-D807
[8]   Epigallocatechin-3-gallate, a green-tea polyphenol, suppresses Rho signaling in TWNT-4 human hepatic stellate cells [J].
Higashi, N ;
Kohjima, M ;
Fukushima, M ;
Ohta, S ;
Kotoh, K ;
Enjoji, M ;
Kobayashi, N ;
Nakamuta, M .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 2005, 145 (06) :316-322
[9]   Disease progression and hepatocellular carcinogenesis in patients with chronic viral hepatitis: a prospective observation of 2215 patients [J].
Ikeda, K ;
Saitoh, S ;
Suzuki, Y ;
Kobayashi, M ;
Tsubota, A ;
Koida, I ;
Arase, Y ;
Fukuda, M ;
Chayama, K ;
Murashima, N ;
Kumada, H .
JOURNAL OF HEPATOLOGY, 1998, 28 (06) :930-938
[10]   ALCOHOLIC LIVER-DISEASE - PATHOLOGICAL, PATHOGENETIC AND CLINICAL ASPECTS [J].
ISHAK, KG ;
ZIMMERMAN, HJ ;
RAY, MB .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1991, 15 (01) :45-66