摘要目的 观察青藤碱对大鼠肝移植缺血再灌注后肝脏树突状细胞功能的影响.方法 应用"二袖套法"建立大鼠肝移植模型,48只BN大鼠分为对照组、低剂量(40 μg/g)和高剂量青藤碱组(80 μg/g),每组16只,术后第3天切取肝脏,分离、纯化肝脏树突状细胞.流式细胞仪对树突状细胞OX62、主要组织相容性复合体Ⅱ(major histocompatibility complex Ⅱ,MHC-Ⅱ)和CD86等分子表型进行分析.RT-PCR测定细胞因子IL-12、IL-1、TNF-a mRNA表达水平,Western blot检测树突状细胞表达的Toll样受体4(Toll-likereceptor4,TLR4).结果 青藤碱处理组树突状细胞呈现不成熟的表型,树突状细胞表面MHC-Ⅱ和CD86表达显著下降.树突状细胞表达IL-12、IL-1、TNF-a mRNA和TLR4蛋白水平明显降低.结论 青藤碱能明显抑制大鼠肝移植缺血再灌注后肝脏树突状细胞成熟和免疫功能.

abstractsObjective To study the effects of Sinomenine on the dendritic cells after hepatic ischemia-reperfusion. Methods Forty-eight BN rats were equally divided into control group, low dose (40 μg/g) and high dose (80 μg/g) of Sinomenine groups after the liver transplantation models were established by two cuff tech-nique. Three days after the orthotopic liver transplantation, the livers were resected, then the dendritic cells were separated and purified. The phenotypes [OX62, major histocompatibility complex Ⅱ (MHC-Ⅱ) and CD86] of dendritic cells were examined by FACS, the expression of IL-12, IL-1, and TNF-a mRNA by RT-PCR, and the expression of Toll-like receptor 4 (TLR4) by Western blot. Results The dendritic cells treated with Sinomenine showed immature phenotypes. The expressions of MHC-Ⅱ and CD86 were significantly deceased. The expressions of IL-12, IL-1, TNF-a mRNA and TLR4 were low. Conclusions Sinomenine can significantly inhibit the maturity and immunologic function of dendritic cells after hepatic ischemia-reperfusion.