흰쥐에서 사염화 탄소(CCl4)에 의한 간섬유화의 유도 = Carbon Tetrachloride(CCl4)- Induced Hepatic Fibrosis in the Rat

다국어 초록 (Multilingual Abstract)

Experimental model of hepatic fibrosis is importent contributions to the understanding of cellular and molecular mechanisms underlying excessive accumulation of extracellular matrix in the liver. Carbon tetrachloride (CCl₄) is one of the oldest and most widely used toxin for experimental induction of hepatic fibrosis in laboratory animals.
In this study, We intended to induce the hepatic fibrosis in the rat by the intragastric CCl₄/ phenobarbtal treatment once a week for 12 weeks and the administration dosage of CCl₄ in each week was determined by the daily body weight change. Liver function and histologic change were examined just after 12-week treatment in group Ia (9 rats, Phenobarbital treatment only) and II (18 rats, CCl₄/phenobarbital treatment), and liver function and the irreversibility o histologic change were examined 12 weeks after 12-week treatment in group Ib (9 rats, phenobarbital treatment only) and III (18 rats, CCl₄/phenobarbital treatment).
1) Death rate after 12-week treatment was 11% in group Ⅰ, 56% in group Ⅱ and 50% in group Ⅲ. and the highest rate was at 1 week. that is 33 o each in group Ⅱ and Ⅲ.
2) Tatal protein, alkaline phosphatase, alanine aminotransferase and portal venous pressure were significantly increased in group Ⅱ compared with that in group Ⅰa, but it was only portal venous pressure that was increased in group Ⅲ than in group Ⅰb,
3) The gross finding of micronodular change was shown in 88% of group Ⅱ, 71% of group Ⅲ, but none of group Ⅰ. The microscopic finding of hepatic fibrosis was found in all of group Ⅱ and Ⅲ, but none of group Ⅰ. The severe form of hepatic fibrosis suggesting cirrhosis was found in group Ⅱ and Ⅲ, 12% and 29% respectively.
In our study, mortality rate was high within 1 week after CCl₄ treatment, which resulted in half survival rate after 12-week treatment. We also experienced the loin rate of severe fibrotic changes in surviving rats. In the future, in order to produce a severe irreversible fibrotic change with low mortality in inducing hepatic fibrosis with CCl₄/phenobarbital treatment in the rat, adequate detemination of the initial dose of CCl₄ and appropriate choice of administration route of CCl₄ were thought to be needed.