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用刀豆蛋白Ａ（ＣｏｎＡ）诱导小鼠建立实验性肝损伤动物模型、观察了该模型血浆丙氨酸转氨酶（ＡＬＴ）、肿瘤坏死因子α（ＴＮＦα）及肝超微结构的变化，证明血浆ＴＮＦα与肝损伤密切相关，肝超微结构的改变突出表现为肝细胞凋亡和坏死。在此基础上研究了地塞米松对该动物模型的影响，结果证明，地塞米松对ＣｏｎＡ诱导的肝损伤具有明显保护作用，与模型组比较可明显抑制ＴＮＦα的产生（Ｐ＜００１），肝超微病理检查未见凋亡或坏死，表明地塞米松对ＴＮＦα产生的抑制作用是保护肝细胞的重要机制。
A mouse model of experimental liver injury was induced by ConA and the changes of plasma ALT, TNFα and hepatic ultrastructure were observed. Proves that plasma TNF α and liver damage are closely related to changes in hepatic ultrastructure highlights the hepatocyte apoptosis and necrosis. Dexamethasone on the basis of this animal model, the results show that dexamethasone ConA-induced liver injury has a significant protective effect, compared with the model group can inhibit TNF @ (P <0 01), no apoptotic or necrotic liver pathological examination showed that dexamethasone on TNF @ inhibition is an important mechanism of protection of liver cells.