摘要
目的 构建接近临床病毒性肝炎发病机制的肝损伤动物模型 ,以便对病毒性暴发性肝炎作进一步的研究。方法 用不同剂量的卡介苗 (BCG)及不同剂量的脂多糖 (LPS)诱导SD大鼠建立急性免疫性肝损伤模型 ,以大鼠血清转氨酶水平变化和肝脏病理学检查等指标作为肝损伤判断标准 ,并以流式细胞仪对该模型的血清中CD3+ 、CD4 + 、CD8+ 细胞百分比计数 ,以ELISA法对TNFα IgG、白介素 (IL 6和IL 10 )水平进行了检测。结果 “BCG +LPS”所造免疫性急性肝损伤模型当以BCG剂量 5× 10 7个活菌 /只及LPS剂量 30 μg kg时ALT升高明显 ,达正常对照 10倍以上 ,AST也较正常对照升高两倍 ;肝脏组织病理损伤中“Ⅲ”级和“Ⅳ”级大于 70 % ,而且其细胞因子水平较正常大鼠升高。对血清中CD3+ 、CD4 + 、CD8+ 细胞百分比也有影响。结论 以“BCG +LPS”所造模型比较成功 ,该模型能充分造成大鼠急性肝损伤 ,且能影响免疫系统 ,与病毒性肝炎的发病机制相似 。
Objective To establish acute immune liver injury model of rats for studying pathogenesis of fulminant viral hepatitis. Method Acute immune liver injury model of rats were induced by injection of different dosages of BCG and LPS. Hepatic injury were assessed by the level of serum transaminase and pathological changes of liver. The percentage of CD3 +,CD4 + and CD8 + cell was determined by flow cytometer. Level of cytokines including TNF α, IL-6 and IL-10 in sera was detected by Enzyme-linked immunoadsordent assay. Result Acute immune liver injury model of rats was successfully established by ip injection of BCG 5×10 7 bacilli/rat and LPS 30 μg/kg body wt, 10 days and 8 h before the assay,respectively. The level of GPT and GOT increased significantly, and pathological changes of “Ⅲ” grade and “Ⅳ” grade were observed in more than 70% assessed liver tissue sections. Level of cytokines including TNF α,IL-6 and IL-10 in sera was higher than that of normal control group. Conclusion Acute immune liver injury model of rats can be established by combined injection of BCG and LPS. The model might be further applied in the research of fulminant viral hepatitis.
出处
《实验动物科学与管理》
2004年第3期15-19,共5页
Laboratory Animal Science & Administration
