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建立小鼠免疫性肝损伤模型，用于治肝炎药的筛选．方法：给小鼠ｉｖ卡介苗（ＢＣＧ）约５×１０７个活菌／０２ｍＬ／只后１０ｄ，再ｉｖ脂多糖（ＬＰＳ）５－１０μｇ／０２ｍＬ／只，测定血清转氨酶水平及肝组织损伤的程度．结果：给小鼠ｉｖＢＣＧ后１０ｄ，再ｉｖＬＰＳ，１２ｈ内ＡｌａＡＴ水平明显升高．肝组织出现炎性细胞浸润、小叶坏死、肉芽肿形成，至１４ｄ肝损伤尚未完全恢复．基因工程干扰素α２ａ、肝细胞生长因子、阿糖腺苷单磷酸、双环醇、联苯双酯、环磷酰胺及氢化泼尼松能减轻ＢＣＧ＋ＬＰＳ所致肝损伤．结论：ｉｖＢＣＧ和ＬＰＳ能引起小鼠免疫性肝损伤，此模型可用于评价治肝炎药的作用．
To establish a mouse model of immune liver injury for the screening of hepatitis drugs. Methods: The mice were treated with BCG (5 × 107 viable cells / 0.2 mL / mouse) for 10 days and then with lipopolysaccharide (LPS) 5-10 μg / 0.2 mL / The extent of damage. Results: After given ivBCG for 10 days, the levels of AlaAT in ivLPS and 12h were significantly increased. Inflammatory cell infiltration, lobular necrosis and granuloma formation occurred in liver tissue. Liver injury was not completely recovered until day 14. Genetic engineering interferon alpha 2a, hepatocyte growth factor, vidarabine monophosphate, bicyclol, bifendate, cyclophosphamide and prednisolone can reduce liver injury caused by BCG + LPS. Conclusion: ivBCG and LPS can cause immunological liver injury in mice. This model can be used to evaluate the therapeutic effect of Hepatitis drugs.