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호암상 수상 기념특강 : Progression and chemoprevention of hepatocellular carcinoma
( Ja June Jang ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.2
Epidemiological and experimental data have demonstrated that the process of carcinogenesis is progressive and multistage in nature. Model systems in animals exhibit this property of cancer development for several organ systems. The rodent liver is one of the most extensively studied models of carcinogenesis. The evolution of hepatic neoplasia is a slow process leading from the normal state via preneoplasia to benign and malignant neoplasia. On the histological level, hepatic preneoplasia usually emerges as foci of altered hepatocytes (FAH) which can be perfectly integrated in the normal liver parenchyma and have no obvious neoplastic nature. The early emergence of FAH seems to be a general phenomenon of hepatocarcinogenesis in all species, no matter how this process has been elicited. In rodent liver treated with various chemical carcinogens, most of phenotypes have been shown to represent successive stages in an ordered sequence of cellular changes, progressing from glycogenic, clear and acidophilic cell foci, through intermediate, mixed and basophilic cell populations, to hepatocellular adenomas and carcinomas, the fast growing variants of which consist of glycogen-poor, basophilic cells. Following curative treatment for hepatocellular carcinoma (HCC), 50%-90% of postoperative death is due to recurrent disease. Chemoprevention, the use of natural or synthetic chemical agents to reverse, suppress or prevent carcinogenesis is considered an important way for confronting HCC. Any agent which can prevent a new HCC from developing in the background of chronic liver diseases after curative treatment, will improve the prognosis of HCC patients.
Jang, Ja June,Cho, Kyung Ja,Lee, Yun Sil,Bae, Jong Hee 濟州大學校 農科大學 動物科學硏究所 1993 動物科學論叢 Vol.8 No.1
The modifying potential of allyl sulfide (As), indole-3-carbinol (13C) and carboxyethyigermanium sesquioxide (GE) on lesion development was examined in a widespectrum initiation model. Groups 1-4 were treated sequentially with diethyl-nitrownine (DEN) (100 mglkg, i.p., single dose), N-methyl-nitrosourea (MNU) (20 mglkg, i.p., four doses at days 2, 5, 8 and 11 ) , and N,Ndibutylnitrosamine (DBN) (0.05% in drinking water during weeks 3 and 4). Groups 5-7 received vehicles without carcinogens during the initiation period. Group 8 served as the untreated control. After this initiating procedure, groups 2-7 were administered a diet containing 0.5% AS or 13C and 0.05% GE. All surviving animals were killed 40 weeks after the beginning of the experiment and the target organs were examined. The induction of GST-P^(+) hepatic foci in rats treated with carcinogens was significantly inhibited by treatment with all three compounds. AS treatment significantly decreased the incidence of hepatic hyperplastic nodules, adenoma of the lung and thyroid, and papillary or nodular hqperplasia of the urinary bladder. Administration of CE also significantly inhibited the development of hepatic nodules and adenoma of the lung and thyroid. However, 13C only inhibited the hyperpbstic nodules of the liver. These results demonstrated that this multi-organ initiation model could be useful in confirming organ-specific modification potential and, in addition, the inhibitory effect of AS, 13C and GE on liver, lung, thyroid and urinaq bladder carcinogenesis.
Thioacetamide 에 의한 간경변에서 Pentoxifylline 투여가 흰쥐의 간 섬유화와 세포주기조절 단백질에 미치는 영향
장자준,장기택,김미란,정인평,이미숙 대한간학회 2001 Clinical and Molecular Hepatology(대한간학회지) Vol.7 No.3
Background: Thioacetamide is a classic hepatotoxic reagent which leads to the reproducible hepatic fibrosis in rats. Thioacetamide-induced fibrosis is an appropriate model for cirrhosis in humans due to the long duration of course and similiar histology. Thioacetamide produces hepatotoxicity through lipid peroxidation but it is unclear whether lipid peroxidation directly correlated with hepatic fibrosis. Pentoxifylline, a derivative of the methylxanthine, showed an antifibrogenic effect in cell cultures of human fibroblasts and some animal models. But this antifibrogenic effect is controversial. Pentoxifylline revealed a hepatoprotective effect in some toxic hepatitis. This hepatoprotective effect seems to influence cell cycle regulatory protein during regeneration. This study aimed to evaluate an effect of pentoxifylline on fibrosis and cell cycle regulatory protein during liver regeneration in thioacetamide-induced rat cirrhosis. Lipid peroxidation assay was compared with collagen content so as to evaluate the correlation with fibrosis. Mothed: Liver cirrhosis was induced by 0.03% oral administration of thioacetamide. Pentoxifylline was administered simultaneously with thioacetamide, The semiquantitative fibrosis index was measured based on histologic finding. Collagen content was estimated by spectrophotometric assay. Activated hepatic stellate cells were counted using α-SMA immunohistochemistry. Malondialdehyde, lipid peroxidation metabolite, was estimated by thiobarbituric acid reactive substance assay. Cell cycle regulatory protein was evaluated by western blot. Results- There was no difference in semiquantitative fibrosis index, collagen content and hepatic stellate cell count between thioacetamide treated rats and simultaneous pentoxifylline treated rats. Lipid peroxidation product was not correlated with collagen content. Western blot showed no difference in cell cycle regulatory protein. Conclusion- Pentoxifylline does not show an antifibrogenic effect in thioacetamide-induced rat cirrhosis, in which thioacetamide induced hepatocellular damage and fibrosis. Lipid peroxidation may be a secondary effect rather than primary mediating mechanism in hepatic fibrosis. (Korean J Hepatol 20017:281-291)