寿胎丸对母胎界面Thl/Th2细胞因子和妊娠结局的影响

Effects of Shoutai pills on expression of Th1/Th2 cytokine in maternal-fetal interface and pregnancy outcome

目的:通过研究寿胎丸对小鼠反复自然流产模型Th1/Th2型细胞因子表达及妊娠结局的影响,探讨寿胎丸在诱导母一胎免疫耐受中的作用机制。方法:设立正常妊娠组(CBA/J×BALB/c)与反复自然流产组(CBA/J×DBA/2),将反复自然流产组孕鼠按怀孕先后顺序随机分为模型组,寿胎丸低、中、高剂量组,从妊娠第1天开始给药,孕14 d后处死孕鼠,计算各组胚胎吸收率,ELISA检测蜕膜及胎盘组织共培养上清细胞因子IL-4,IL-10,IFN-γ,TNF-α的含量。结果:模型组的胚胎吸收率模型高于正常妊娠组,寿胎丸中、高剂量能显著降低反复自然流产孕鼠的胚胎吸收率,寿胎丸低、中、高剂量组均可降低反复自然流产小鼠母胎界面IFN-γ和TNF-α的表达,差异具有统计学意义(P<0.05),与正常妊娠组比较,差异无统计学意义;寿胎丸中、高剂量组可升高反复自然流产小鼠母胎界面IL-4,IL-10的表达,差异具有统计学意义(P<O.05),与正常妊娠组比较,差异无统计学意义。结论:寿胎丸保胎机制可能是通过调节母-胎界面局部Thl/Th2型细胞因子的表达,形成维持正常妊娠所需的Th2型免疫偏倚,诱导母-胎免疫耐受,维持妊娠。

Objective： To evaluate its mechanism of inducing the maternal-fetal immune tolerance by studying the effects of Shoutai pills on the expression of Th1/Th2 cytokine andpregnancy in maternal-fetal interfaee of mice with recurrent spontaneous abortion（RSA）.Method： The normal pregnancy and RSA model were respectively induced with CBA/J×BALB/c and CBA/J ×DBA/2.The mice with RSA were randomly divided into model group and low,middle and high dose groups of Shoutai pills.The mice were killed in 14 days after administration and embryo resorption rate was counted and their decidual and placental tissues were co-cultured to detect the expressions of IL-4,IL-10,IFN-γ and TNF-α with ELISA.Resuit： The embryo resorption rate of the model group was significantly higher than the normal pregnancy,middle and high dose groups of Shoutai pills could decreased the embryo resorption rate of the mice with RSA（P〈0.05）.All the doses in 3 groups of Shoutai pills could decreased the expression of IFN-γ and TNF-α（P〈0.05） and there was no obvious difference between normal pregnancy group and all groups of Shoutai pills.Middle and high doses of Shoutai pills could increased the expression of IL-4 and IL-10（P〈0.05） and there was no obvious differences between normal pregnancy and high dose group of Shoutai pills.Conclusion： The mechanism about Shoutai pills can change Th1 /Th2 cytokine towards Th2 bias,which induced the maternal-fetal immune tolerance.