当归多糖对刀豆蛋白A所致小鼠免疫性肝损伤的保护作用

Protective Effects of Angelica sinensis Polysaccharide on Immunological Liver Injury Induced by Concanavalin A in Mice

目的:研究当归多糖对刀豆蛋白A(ConA)诱导的小鼠免疫性肝损伤的保护作用,并探讨其可能的作用机制。方法:60只NIH小鼠随机分为6组,分别为正常对照组、模型组、联苯双酯阳性对照组及当归多糖高、中、低剂量组,每组10只。各组分别于首日上、下午和第2日下午各灌胃给药1次,正常对照组与模型组给予等容积生理盐水。末次给药后4 h,除正常对照组外,其余各组小鼠均一次性尾静脉注射ConA 20 mg/kg诱导小鼠免疫性肝损伤,禁食不禁水8 h后称量体质量,摘眼球采血,脱颈椎处死动物,并计算小鼠的胸腺、肝脏、脾脏系数(mg/10g),检测小鼠血清丙氨酸氨基转移酶(ALT)、门冬酸氨基转移酶(AST)、总胆红素(TB)、一氧化氮(NO)的含量以及肝组织匀浆中肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)和干扰素γ(IFN-γ)的含量,HE染色切片观察肝组织病理学变化。结果:当归多糖与联苯双酯均可显著改善免疫性肝损伤小鼠的胸腺、肝脏、脾脏系数(P<0.05);降低血清中ALT、AST、TB、NO的含量(P<0.05)以及肝组织匀浆中TNF-α、IL-1β、IFN-γ的含量(P<0.05);当归多糖组和联苯双酯组肝脏病理改变明显减轻(P<0.05)。结论:当归多糖对免疫性肝损伤具有显著的保护作用,其高剂量作用效果与联苯双酯相当,并且在实验剂量范围内显著出剂量依赖性。抑制T淋巴细胞的活化和IFN-γ、TNF-α、IL-1β、NO的释放可能是其作用主要的机制。

Objective：To investigate the protective effects of Angelica sinensis polysaccharide on immunological liver injury induced by concanavalinA（ConA）. Methods：Sixty NIH mice were randomly divided into 6 groups as normal group, model group, biphenyl group, Angelica sinensis polysaccharide high does group, Angelica sinensis polysaccharide middle dose group and Angelica sinensis polysaccharide low dose group. Immunological liver injury in mice was induced by ConA （20 mg/kg） by injection via tail vein, the control group received saline alone. In the treatment groups, each group was administrated via gavage daily. The control group was given equal volume of saline. Liver index, thymus index and spleen index, contents of serum ALT, AST, TB and NO in serum and TNF- α,IL-1β,ITN-γ in liver homogenate were measured. Results：Angelica sinensis polysaccharide remarkably increased the levels of liver index, thymus index and spleen index, decreased the contents ALT, AST, TB and NO levels in serum, and TNF-α,IL-1β,ITN-T in liver homogenate（ P 〈 0. 05 ）. Conclusion：Angelica simesis polysaccharide haride can obviously protect immunological injury liver in mice and between the dose range of 30 - 120 mg/kg in a dose-dependent manner. Its mechanism may be relate to inhibiting T lymphocyte activity and ITN-γ, TNF-α, IL-1β,NO release.