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本研究利用丙酸杆菌和内毒素建立了肝坏死动物模型。其结果：①２４小时死亡率为８３％（２０／２４）。肝组织学检查所见肝小叶中有大量单核吞噬细胞浸润，并出现大片肝坏死；②脾细胞对ＰＨＡ和ＣｏｎＡ反应明显降低；③肝枯否氏细胞肿瘤坏死因子和白细胞介素１生成能明显增高；④白细胞介素２不能调节脾细胞对ＰＨＡ的反应。上述结果说明此模型与免疫异常有着密切关系，是研究肝坏死免疫发生机理的较理想模型。
In this study, animal models of hepatic necrosis were established using propionibacteria and endotoxin. The results: ①24-hour mortality rate was 83% (20/24). Hepatic histological examination revealed a large number of mononuclear phagocyte infiltration in the hepatic lobules with massive necrosis of the liver; ② The response of spleen cells to PHA and ConA was significantly reduced; ③ The production of TNF-α and IL-1 Significantly increased; ④ interleukin 2 can not regulate spleen cells response to PHA. The above results show that this model is closely related to immune abnormalities and is a more ideal model to study the mechanism of liver necrosis.