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目的探讨细胞因子信号传导负调控因子3(SOCS3)在妊娠期肝内胆汁淤积症(ICP)发病中的作用及可能的调节机制。方法选取正常孕妇(A组,18例)、轻型ICP孕妇(B组,18例)及重型ICP孕妇(C组,19例),分离获得其胎盘来源的单核-巨噬细胞,用ELISA法检测细胞培养上清液中TNF-α、IL-10、IL-12水平,RT-PCR及Western blot法分别检测SOCS3mRNA及蛋白水平的表达,TransAMTM核蛋白定量分析法检测NF-κB/p65的水平。结果与A组比较,B、C组高分泌TNF-α、IL-12,低表达SOCS3,NF-κB/p65的量增多(P<0.01),且C组较B组更明显(P<0.01);三组IL-10的分泌水平均较低。结论 ICP孕妇胎盘组织内以Th1型细胞因子(IL-12)占主导,而Th2型细胞因子(IL-10)的水平明显减低。妊娠期ICP患者Th1/Th2型细胞因子的失衡可能与SOCS3和NF-κB/p65的活化调节有关。
Objective To investigate the role of cytokine signaling negative regulator 3 (SOCS3) in the pathogenesis of intrahepatic cholestasis of pregnancy (ICP) and its possible regulatory mechanism. Methods Normal pregnant women (group A, 18 cases), mild ICP pregnant women (group B, 18 cases) and heavy ICP pregnant women (group C, 19 cases) were selected and their placenta derived mononuclear macrophages were isolated. The levels of TNF-α, IL-10 and IL-12 in cell culture supernatants were detected. The expression of SOCS3 mRNA and protein were detected by RT-PCR and Western blot respectively. The levels of NF-κB / p65 . Results Compared with group A, the secretion of TNF-α, IL-12, SOCS3 and NF-κB / p65 were significantly increased in group B and C (P <0.01) ); Three groups of IL-10 secretion levels were lower. CONCLUSION: Th1 cytokine (IL-12) is predominant in the placenta of ICP pregnant women, while the level of Th2 cytokines (IL-10) is significantly lower in ICP pregnant women. The imbalance of Th1 / Th2 type cytokines in ICP patients during pregnancy may be related to the regulation of SOCS3 and NF-κB / p65 activation.