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为探讨ＴＮＦ－α在刀豆蛋白Ａ（ＣｏｎＡ）诱导的肝损伤中的作用，在ＣｏｎＡ诱导的小鼠急性肝损伤模型上，观察血浆ＴＮＦ－α含量、ＡＬＴ活性、光镜和电镜下肝组织病理变化及应用抗ＴＮＦ－α单抗的肝损伤阻断作用。结果发现，与正常对照组比较，模型组ＴＮＦ－α、ＡＬＴ明显增高［分别为（０．１９±０．０６）ｎｇ／ｍｌ，（１４１４±５６７）Ｕ／Ｌ，均为Ｐ＜０．０１］，肝损伤在光镜、电镜下表现为肝细胞凋亡和坏死；抗ＴＮＦ－α单抗组的ＴＮＦ－α、ＡＬＴ分别较模型组和无关单抗组明显降低，未见肝细胞凋亡和坏死。结果表明：肝细胞凋亡可能为ＣｏｎＡ诱导肝细胞死亡的机制；ＴＮＦ－α在ＣｏｎＡ性肝损伤模型中起重要的介导作用；抗ＴＮＦ－α单抗可以阻断ＣｏｎＡ性肝损伤的发生，即有肝细胞保护作用。
To investigate the role of TNF-α in ConA-induced liver injury, the levels of TNF-α and ALT in plasma of ConA-induced acute liver injury model were observed. Liver tissue Pathological changes and the blocking effect of anti-TNF-α monoclonal antibody on liver injury. The results showed that the levels of TNF-α and ALT in the model group were significantly higher than those in the normal control group [(0.19 ± 0.06) ng / ml and (1414 ± 567) U / L, respectively, P <0.01 ], Liver injury under light and electron microscopy showed hepatocyte apoptosis and necrosis; TNF-α and anti-TNF-α monoclonal antibody group were significantly lower than the model group and non-related monoclonal antibody group, no apoptosis of hepatocytes And necrosis. The results showed that hepatocyte apoptosis may be the mechanism of ConA-induced hepatocyte death; TNF-α may play an important mediating role in ConA-induced liver injury; anti-TNF-α monoclonal antibody may block ConA-induced liver injury, That is, hepatocyte protective effect.