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本研究采用ＣｏｎＡ诱导，建成小鼠肝损伤模型，并检测其血浆肿瘤坏死因子－α（ＴＮＦ－α）含量的变化，发现模型组鼠血浆ＴＮＦ－α含量为０．１９±０．０６ｎｇ／ｍｌ，而正常对照组未检出ＴＮＦ－α，二者比较有极显著差异（Ｐ＜０．００１）。预先注射抗Ｔａｃ单克隆抗体可减少ＣｏｎＡ注射后小鼠ＴＮＦ－α的产生，与模型组比较（分别为０．０３±０．０２和０．１９±０．０６），二者有极显著差异（Ｐ＜０．００１），而且注射抗Ｔａｃ单抗组无肝损伤发生。上述结果表明，ＣｏｎＡ诱导的肝损伤与ＴＮＦ－α等的介导有关，抗Ｔａｃ单克隆抗体对ＣｏｎＡ诱导的肝损伤有保护作用。
In this study, ConA-induced mouse liver injury model was established and the changes of plasma tumor necrosis factor-α (TNF-α) levels were determined. The plasma levels of TNF-α in the model group were 0.19 ± 0.06ng / ml , While no TNF-α was detected in the normal control group. There was a significant difference between the two groups (P <0.001). Pre-injection of anti-Tac monoclonal antibody decreased the production of TNF-α in mice after ConA injection compared with the model group (0.03 ± 0.02 and 0.19 ± 0.06, respectively), with significant difference between the two (P <0.001), and no liver injury occurred in the anti-Tac mAb group. The above results show that ConA-induced liver injury is mediated by TNF-α and other anti-Tac monoclonal antibodies have a protective effect on ConA-induced liver injury.