摘要
目的探讨茵陈多糖对妊娠胆汁淤积大鼠Th1/Th2细胞免疫平衡的调节作用。方法 32只妊娠SD大鼠随机分为对照组,模型组,低剂量组及高剂量组,妊娠16周采用苯甲酸雌二醇注射法建立妊娠胆汁淤积大鼠模型,造模成功后低剂量组(50mg/Kg.d-1)及高剂量组(100mg/Kg.d-1)分别给予茵陈多糖干预,1周后采用流式细胞技术检测各组大鼠静脉血Th1、Th2及Th1/Th2比值变化,采用比色法检测各组大鼠血清IL-6、TNF-α及IFN-γ表达水平变化。结果茵陈多糖干预1周后,模型组Th1较对照组上升,Th2较对照组下降,Th1/Th2比值升高,高剂量组及低剂量组Th1较模型组下降,Th2较模型组上升,Th1/Th2比值较模型组降低,高剂量组及低剂量组之间Th1、Th2及Th1/Th2比值差异有统计学意义。模型组IL-6、TNF-α、IFN-γ较对照组升高,高剂量组及低剂量组IL-6、TNF-α、IFN-γ较模型组降低。高剂量组及低剂量组间IL-6、TNF-α和IFN-γ水平差异有统计学意义。结论茵陈多糖能够对妊娠胆汁淤积大鼠Th1/Th2免疫失衡进行调节,减轻免疫损伤。
Objective To investigate the regulating action of artemisiae capillaries polysaccharides on immunologic balance of Th1/Th2 in rats with intrahepatic cholestasis of pregnancy(ICP).Methods Thirty-two SD rats were randomly divided into control groups(CG),model groups(MG),high-dose groups(HG)and low-dose roups(LG)with random digits table,animal medol of ICP were made with injecting estradiol benzoate 16 weeks after gestation of the.rats in HG(100mg/Kg.d-1)and LG(50mg/Kg.d-1)were interfered with artemisiae capillaries polysaccharides,The Ratios of Th1,Th2 and Th1/Th2 in venous blood were detected with flow cytometer,and level of IL-6,TNF-αand IFN-γ in serum were also detected with colorimetric method after a week.Results A week after artemisiae capillaries polysaccharides inversion,the level of Th1 was higher and that the Th2 was lower and ratio of Th1/Th2 was higher in MG than in CG,The level of Th1 was lower and that of the Th2 was higher and the ratio of Th1/Th2 was lower in LG and HG than in MG,showing significant difference between the level of LG and HG.The levels of serumIL-6,TNF-αand IFN-γin were higher in MG than in CG,while the Levels of IL-6,TNF-αand IFN-γ were lower in HG and LG than in MG,also showing significant difference.Conclusions Artemisiae capillaries polysaccharides could regulate the immune balance of Th1/Th2 in rats with ICP,and lessen immunologic injury.
出处
《中国热带医学》
CAS
2013年第3期267-269,共3页
China Tropical Medicine
基金
广东省中医药管理局立项资助项目(No.20121256)
关键词
茵陈
多糖
妊娠胆汁淤积
Th细胞免疫
免疫损伤
Artemisiae capillaries
Polysaccharides
ICP
Th cellular immunity
Iimmunologic injury