中文摘要：

目的研究松果菊苷对刀豆蛋白A（Con A）诱导的急性肝损伤小鼠的保护作用以及对细胞外组蛋白水平的影响,并初步探讨其可能机制。方法将野生型C57BL/6（B6）小鼠随机分为正常对照组（n=6）、Con A染毒组（n=8）和松果菊苷＋Con A组（n=8）。Con A染毒组小鼠经尾静脉注射Con A（30mg/kg）诱导急性肝损伤,松果菊苷＋Con A组小鼠先给予松果菊苷（50mg/kg）连续灌胃3d,然后再给予Con A染毒;正常对照组仅给予生理盐水。计算各组小鼠的生存率,HE染色观察肝损伤情况,ELISA法检测血清细胞外组蛋白表达情况,高效液相芯片系统测定细胞因子IL-1β、IL-6、IL-10和TNF-α水平的变化。结果与正常对照组相比,Con A染毒组小鼠肝损伤严重,病理学观察可见大量肝细胞凋亡变性坏死,血清ALT、AST水平明显升高,血清中细胞外组蛋白和细胞因子IL-1β、IL-6、IL-10和TNF-α水平均明显升高（P〈0.01）。与Con A染毒组比较,松果菊苷＋Con A组生存小鼠明显增多,肝损伤程度亦减轻;细胞外组蛋白、IL-1β、IL-6、IL-10和TNF-α水平均显著低于染毒组,差异有统计学意义（P〈0.05或P〈0.01）。结论松果菊苷能明显减轻Con A诱导的小鼠急性肝损伤,其机制可能与降低血清中细胞外组蛋白及肝损伤相关的细胞因子水平有关。

英文摘要：

Objective To investigate the effect of echinacoside on the protection of acute liver injur y induced by concanavalin A（Con A） in mice and on the extracellular histones. Methods Male C57BL/6（B6） mice were randomly divided into three groups： control group（n=6）, which received saline only; Con A-treated group（n=8）, which were given Con A（30mg/kg） viatail vein; echinacoside plus Con A-treated group（n=8）, which were treated with echinacoside solutions by gavage at a dose of 50mg/kg for 3 days before Con A injection. At 16 h after Con A treatment, all mice were sacrificed to collect blood and tissue samples for analysis of hepatic function, pathological indexes, as well as extracellular histones and the relevant inflammatory cytokines. Results Acute liver injury in mice was induced by Con A administration as demonstrated by elevated serum ALT, AST levels and severe pathological changes. Echinacoside plus Con A-treated mice showed significantly lower levels of ALT and AST and milder liver injury than that in Con A-treated mice（P0.01）. The number of mice survived in echinacoside plus Con A-treated group was more than that in Con A-treated group. Moreover, the levels of extracellular histones and IL-1, IL-6, IL-10 and TNF-α were markedly decreased in echinacoside plus Con A-treated mice as compared to those in Con A-treated mice（P0.01）. Conclusions Echinacoside may act an obvious protective effect against acute liver injury induced by Con A, and it might be due to its inhibitory effect on pro- inflammatory mediators including cytokines and lowering of extracellular histones.