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[酒精和四氯化碳诱导的肝纤维化实验模型:脂多糖能否预防酒精和四氯化碳诱导的肝损伤?]

[An experimental model of hepatic fibrosis induced by alcohol and CCl4: can the lipopolysaccharide prevent liver injury induced by alcohol and CCl4?].

作者信息

Chae Hee Bok, Jang Lee Chan, Park Seon Mee, Son Bo Ra, Sung Rohyun, Choi Jae Woon

机构信息

Department of Internal Medicine, College of Medicine and Medical Research Institute, Chungbuk National University, Cheongju, Korea.

出版信息

Taehan Kan Hakhoe Chi. 2002 Jun;8(2):173-8.

Abstract

BACKGROUND/AIMS: It is well known that alcohol enhances the toxicity of CCl4. We tried to establish an alcoholic liver cirrhosis model by administration of alcohol and CCl4 to rats. We also wanted to know the hepatoprotective effect of low doses of lipopolysaccharide(LPS) in this animal model.

METHODS

Of 20 female adult rats, 8 were ingested with alcohol ad libitum(group 1) Another 6 were ingested with 10% alcohol and 50% 1mL/kg CCl4 intragastrically by Sonde twice a week(group 2) The remaining 6 were ingested with 10% alcohol, CCl4, and 0.1mg/kg LPS intraperitoneally twice a week(group 3) The fibrosis was evaluated semiquantitatively on a scale of 0(none) to 3(cirrhosis).

RESULTS

  1. After 10 weeks, septal fibrosis or cirrhosis was produced in 9 out of 12 rats in groups 2 and 3 but there was no fibrotic change in group 1. 2) There was no significant difference in pathological grading between groups 2 and 3.

CONCLUSIONS

Hepatic fibrosis or cirrhosis can be sufficiently induced by alcohol and repetitive CCl4 ingestion for 10 weeks. We can not prove the hepatoprotective effect of low dose LPS by semiquantitative evaluation of pathological grading.

摘要

背景/目的:众所周知,酒精会增强四氯化碳的毒性。我们试图通过给大鼠灌胃酒精和四氯化碳来建立酒精性肝硬化模型。我们还想了解低剂量脂多糖(LPS)在该动物模型中的肝脏保护作用。

方法

20只成年雌性大鼠中,8只随意饮用酒精(第1组)。另外6只每周通过探条经胃内给予10%酒精和50% 1mL/kg四氯化碳两次(第2组)。其余6只每周经腹腔给予10%酒精、四氯化碳和0.1mg/kg LPS两次(第3组)。纤维化程度采用0(无)至3(肝硬化)的半定量评分。

结果

1)10周后,第2组和第3组12只大鼠中有9只出现间隔纤维化或肝硬化,而第1组无纤维化改变。2)第2组和第3组之间病理分级无显著差异。

结论

连续10周摄入酒精和反复给予四氯化碳可充分诱导肝纤维化或肝硬化。通过病理分级的半定量评估,我们无法证明低剂量LPS的肝脏保护作用。

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