姚晓敏, 李宏伟, 曲均革, 崔相一. 刀豆蛋白A引起小鼠免疫性肝损伤机制研究[J]. 蚌埠医学院学报, 2011, 36(5): 445-447.
    引用本文: 姚晓敏, 李宏伟, 曲均革, 崔相一. 刀豆蛋白A引起小鼠免疫性肝损伤机制研究[J]. 蚌埠医学院学报, 2011, 36(5): 445-447.
    YAO Xiao-min, LI Hong-wei, QU Jun-ge, CUI Xiang-yi. The related mechanism of immunological liver injury induced by concanavalin A in mice[J]. Journal of Bengbu Medical College, 2011, 36(5): 445-447.
    Citation: YAO Xiao-min, LI Hong-wei, QU Jun-ge, CUI Xiang-yi. The related mechanism of immunological liver injury induced by concanavalin A in mice[J]. Journal of Bengbu Medical College, 2011, 36(5): 445-447.

    刀豆蛋白A引起小鼠免疫性肝损伤机制研究

    The related mechanism of immunological liver injury induced by concanavalin A in mice

    • 摘要: 目的:建立刀豆蛋白A(Con A)引起小鼠免疫性肝损伤模型,并考察其损伤机制。方法:ICR小鼠随机分为正常对照组和Con A模型组,每组10只。Con A模型组小鼠尾静脉注射Con A2.5 mg·ml-1·kg-1,对照组给予等体积生理盐水。造模后8 h断头处死小鼠,分别取肝脏和血液,采用生化法测定小鼠血清丙氨酸氨基转移酶(ALT)和天冬氨酸转移酶(AST)水平,苏木精-伊红染色法测定肝组织病理学改变,ELISA法测定血清肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)含量。结果:与正常对照组比较,Con A模型组小鼠血清ALT和AST水平均显著升高(P<0.01),肝细胞明显坏死,伴炎细胞浸润,同时血清中TNF-α和IFN-γ含量亦均显著升高(P<0.01)。结论:尾静脉注射Con A 2.5 mg·ml-1·kg-1可建立免疫性肝炎模型,其损伤机制与炎症因子表达相关。

       

      Abstract: Objective: To establish the model of immunological liver injury in mice and investigate the related mechanisms.Methods: Twenty mice were randomly divided into normal control and Con A groups,10 in each.Mice of Con A group were injected with Con A 2.5 mg·ml-1·kg-1 by vena caudalis,and sacrificed after 8 hours.The blood and liver tissue were collected to examine ALT and AST levels spectrophotometrically,the histopathology changes were measured by HE method,and serum TNF-α and IFN-γ contents were measured by ELISA.Results: Compared with normal control group,serum ALT and AST levels were significantly elevated,serum TNF-α and IFN-γ contents were markedly increased(P<0.01).Meanwhile,hepatic necrosis and neutrophil infiltration also occured in Con A group.Conclusions: The model of immunological liver injury in mice was established by vena caudalis injection of Con A,the related mechanism is partially due to regulating the expressions of inflammatory cytokines.

       

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