Ornithine decarboxylase prevents methotrexate-induced apoptosis by reducing intracellular reactive oxygen species production

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Title:	Ornithine decarboxylase prevents methotrexate-induced apoptosis by reducing intracellular reactive oxygen species production
Authors:	Huang, CC;Hsu, PC;Hung, YC;Liao, YF;Liu, CC;Hour, CT;Kao, MC;Tsay, GJ;Hung, HC;Liu, GY
Contributors:	醫學院醫學系;Chung Shan Med Univ, Inst Immunol, Taichung, Taiwan;Tzu Hui Inst Technol, Pingtung, Taiwan;Da Chien Gen Hosp, Dept Med, Miaoli, Taiwan;Kaohsiung Med Univ, Inst Biochem, Kaohsiung, Taiwan;Natl Chung Hsing Univ, Dept Life Sci, Taichung 40227, Taiwan;China Med Univ, Sch Med, Taichung, Taiwan;Chung Shan Med Univ Hosp, Dept Internal Med, Taichung, Taiwan
Date:	2005
Issue Date:	2010-09-24 14:51:55 (UTC+8)
Publisher:	SPRINGER
Abstract:	The aim of this study was to investigate the effects of aqueous extract of Anoectochilus formosanus (AFE) on liver fibrogenesis in carbon tetrachloride (CCl4)-induced cirrhosis. Fibrosis was induced in rats by oral administration of CCl4 (20%, 0.5 ml/rat, p.o.) twice a week for 8 weeks. AFE (0.5 and 2.0 g/kg, p.o., daily for 8 weeks) was administered to rats simultaneously. AFE showed reducing actions on the elevated levels of GOT and GPT caused by CCl4. Liver fibrosis in rats induced by CCl4 led to the drop of serum albumin concentration; the AFE increased the albumin concentration. The CCl4-induced liver fibrosis markedly caused liver atrophy and splenomegalia, while AFE increased the liver weight, and decreased the spleen weight. The CCl4-induced liver fibrosis decreased the protein content, and increased collagen contents in rat's liver. AFE significantly increased the contents of protein and reduced the amount of collagen in the liver. In CCl4-treated rats, glutathione concentrations of liver were not affected. AFE significantly increased liver glutathione concentrations. All these results clearly demonstrate that AFE can reduce the liver fibrogensis in rats induced by CCl4. (c) 2005 Elsevier GmbH. All rights reserved.
Relation:	APOPTOSIS 10(4):895-907
Appears in Collections:	[School of Medicine] Journal articles

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