ConA诱导小鼠肝损伤模型的发病机制  

The Mechanism of Concanavalin A induced Liver Injury

作　　者：胡水清[1] 黄依雯[1] 秦伟[1] 柳娟[1] 徐辰迪[1] 孔方圆[1] 张雁云[1] 

机构地区：[1]上海交通大学医学院上海市免疫学研究所,上海200025

出　　处：《中国血液流变学杂志》2007年第1期159-162,共4页Chinese Journal of Hemorheology

基　　金：国家自然科学基金(30670911);上海市科委重点项目(03JC14085);上海市重点学科建设项目资助(T0206);上海市科委创新团队项目(04DZ14902);上海交通大学医学院211工程

摘　　要：刀豆蛋白A(Con A)诱发的小鼠急性肝损伤是T淋巴细胞介导的肝损害模型之一,很好地模拟了人类病毒性肝炎、自身免疫性肝病等疾病。其特征是在很短时间内小鼠肝脏有大量中性粒细胞、巨噬细胞、T细胞等炎症性细胞浸润,同时血液中转氨酶水平大量升高。大量的促炎细胞因子(白介素4,肿瘤坏死因子α和γ-干扰素等)、趋化性因子(骨桥蛋白)、趋化因子受体(趋化因子受体5)参与了该模型的发病过程。此外,凋亡机制在该模型的肝脏损伤中也发挥了非常重要的作用。该文就这一肝损害模型的特点和发病机制的研究进展作综述。Concanavalin A（Con A） induced liver injury is one of the mouse models of T cell-dependent liver failure which resembles virus-induced immune injury of liver and autoimmune liver disease. It is characterized by fast inflammation of the liver with obvious infiltration ofneutrophils, macrophages and T cells along with a marked and simultaneous increase of the transaminases in the blood. Besides, it has also been shown that Con A-induced hepatitis involves a lot of pro-inflammatory cytokines（IL-4,TNF- α and IFN-γ）, chemokines（osteopontin） and chemokine receptors（CCRS）.In addition, apoptosis may also play important roles in the development of liver failure. This paper mainly reviews the characteristics and mechanisms of the liver injury model induced by concanavalin A.

关 键 词：刀豆蛋白A 转氨酶 淋巴细胞 肝炎 

分 类 号：R392.32[医药卫生—免疫学]