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 ,可以用其对病毒性暴发性肝炎进行研究 Objective To construct an animal model of liver injury that is close to the pathogenesis of clinical viral hepatitis for further study on viral fulminant hepatitis. Methods Acute immunological liver injury models were induced in SD rats with different doses of BCG and different doses of lipopolysaccharide (LPS). Serum aminotransferase levels and liver pathology were used to determine the severity of liver injury in SD rats. The percentages of CD3 +, CD4 + and CD8 + cells in the serum of the model were counted by flow cytometry, and the levels of TNFα IgG, interleukin (IL 6 and IL 10) were detected by ELISA. Results The model of autoimmune acute liver injury induced by “BCG + LPS” showed a significant increase of ALT when the dose of BCG was 5 × 10 7 viable cells / LPS and 30 μg kg of LPS, which was more than 10 times higher than that of normal control Control doubled; liver tissue pathological lesions “Ⅲ” and “Ⅳ” level is greater than 70%, and its cytokines levels higher than normal rats. The percentage of CD3 +, CD4 + and CD8 + cells in serum also has an impact. Conclusion The successful model of “BCG + LPS” is successful. This model can induce acute liver injury in rats and affect the immune system. Similar to the pathogenesis of viral hepatitis, it can be used to study viral fulminant hepatitis