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本文采用Ｓ１００肝抗原四次免疫Ｗｉｓｔａｒ大鼠后，成功地建立了实验性自身免疫性肝炎（ＥＡＨ）动物模型、并在此基础上对其发病机制进行了初步探讨，通过脾淋巴细胞增殖试验、血清谷丙转氨酶（ＡＬＴ）及血清免疫球蛋白测定，结果显示、自身免疫损害病理改变出现在第一次免疫后一周，５个月后仍有病理损伤。血清ＡＬＴ与病理损害过程一致、血清ＩｇＧ在免疫后第二周升高。实验结果提示Ｓ１００可以诱导典型的ＥＡＨ。此模型可成为研究自身免疫性肝炎发病机制的重要工具。
In this study, we successfully established an animal model of experimental autoimmune hepatitis (EAH) after four immunizations of Wistar rats with S100 liver antigen. On the basis of this, we made a preliminary study on the pathogenesis of Wistar rats. Through the splenic lymphocyte proliferation test, Serum alanine aminotransferase (ALT) and serum immunoglobulin measured, the results showed that pathological changes in autoimmune lesions appeared in the first immunization week, five months after the still pathological damage. Serum ALT consistent with the pathological damage, serum IgG in the second week after immunization increased. The experimental results suggest that S100 can induce typical EAH. This model can be an important tool for studying the pathogenesis of autoimmune hepatitis.