双氢青蒿素保护刀豆蛋白A诱导的小鼠肝损伤及机制探讨

目的研究双氢青蒿素(dihydroqinghaosu,DQHS)对刀豆蛋白A(concanavalin A,ConA)诱导的小鼠免疫性肝损伤的保护作用及可能机制。方法小鼠尾静脉注射ConA建立肝损伤模型;改良赖式法和ELISA法分别测定DQHS预给药对该模型小鼠血浆转氨酶和TNF-α水平的影响;MTT法检测DQHS对ConA诱导体外小鼠脾淋巴细胞增殖的影响;RT-PCR检测DQHS对LPS刺激的RAW264.7巨噬细胞IL-1β和TNF-αmRNA表达水平的影响。结果与模型组比较,DQHS 40μg.g-1给药组可降低ConA诱导的肝损伤小鼠血浆转氨酶水平,各DQHS组均可降低该小鼠血浆TNF-α水平;DQHS 40μmol.L-1和100μmol.L-1处理组能抑制ConA诱导的体外脾淋巴细胞增殖,减少LPS刺激的巨噬细胞炎症因子IL-1β和TNF-αmRNA的表达。结论DQHS对ConA诱导的小鼠免疫性肝损伤有保护作用,该作用可能通过抑制脾淋巴细胞增殖和巨噬细胞相关炎症细胞因子表达来实现。

The protective effect of DQHS on ConA-induced liveRinjury in mice and its mechanism

Aim To investigate the protective effect of dihydroqinghaosu(DQHS) on Concanavalin A(ConA)-induced immunologic liver injury in mice and the potential mechanism.Methods Mice liver injury model was induced by ConA vena caudalis injection;transaminases and TNF-α levels with DQHS pretreatment were measured by Improved Reitman-Frankel assay and ELISA methods;the effect of DQHS on ConA-induced proliferation of lymphocyte was tested by MTT method in vitro;the effect of DQHS on LPS-stimulated IL-1β and TNF-α mRNA expression in RAW264.7 macrophage was detected by RT-PCR method.Results Compared with the model group,DQHS(40 μg·g-1) pretreatment could reduce transaminases levels and in all groups DQHS pretreatment could reduce the TNF-α level in ConA-induced liver injury;DQHS(40 μmol·L-1 and 100 μmol·L-1) could inhibit the proliferation of ConA-stimulated lymphocyte and reduce the expression of IL-1β and TNF-α in LPS-stimulated macrophage in vitro.Conclusions DQHS has protective effect on ConA-induced liver injury.This may be implemented by inhibiting the proliferation of lymphocyte and decreasing the release of inflammatory factors in macrophage.