首页> 中文期刊>河北联合大学学报(医学版) >丙泊酚诱导 LPS 刺激的树突细胞向调节性树突细胞分化的研究

丙泊酚诱导 LPS 刺激的树突细胞向调节性树突细胞分化的研究

     

摘要

Objective To explore the possibility of propofol on promoting DC to CD11clow CD45RBhigh DC subsets which produce IL-10.Methods Purification of splenic DCs cells in C57BL/6 mice were administrated by magnetic beads sorting.Then,these splenic DCs cells were divided into six groups:the NS group,LPS 1μg/mL(L group),LPS 1μg/mL+Propofol 5μg/mL (P1 group)、LPS 1μg/mL+Propofol 10μg/mL(P2 group)、LPS1μg/mL+ Propofol 20μg/mL(P3 group).Cultured after 24 hours,flow cytometry was used to determine expressions of DC surface molecules including CD40, CD80,CD86,I-a/e in six groups.IL-10 levels in DC culture supernatants were determined by sandwich enzyme-linked immunosorbent assays (ELISA).Results Compared with the results of the NS group, the expression of CD40,CD80,CD86,I-a/e as well as IL-10 secretion level was increased in the L group.Compared with the results of the L group,propofol could markedly decrease the expression of CD80、CD40 and I-a/e while enhancing the expression of CD86 as well as IL-10 secretion level.Besides, the enhancement of IL-10 secretion level hinges upon the rise of propofol concentration.Conclusion Propofol can inhibit the early inflammatory response by promoting DC to CD11c lowCD45RBhigh DCs differentiation and adjusting the secretion of IL-10.%①目的探讨丙泊酚(Propofol)诱导脂多糖(LPS)刺激的树突细胞(DC)向分泌白细胞介素(IL)-10的树突细胞亚群-CD11clow CD45RBhigh DC 分化。②方法采用磁珠分选技术获得 C57BL/6小鼠脾脏树突细胞,将提取的 DC 分为6个组,分别加入同体积的生理盐水(NS 组),LPS 1μg/mL(L 组), LPS 1μg/mL+5μg/mL 丙泊酚(P1组)、LPS 1μg/mL+10μg/mL 丙泊酚(P2组)、LPS 1μg/mL +20μg/mL 丙泊酚(P3组)后进行培养24小时,分别用流式细胞仪检测各组细胞表面分子 CD40、CD80、CD86、I-a/e 的表达情况,采用 ELISA 法检测培养液中 IL-10的含量。③结果与 NS 组相比,L 组 DC表面分子 CD40、CD80、CD86和 I-a/e 的表达均明显增强(P <0.05),同时 IL-10的分泌升高;而与 L 组相比,较大剂量丙泊酚能显著降低 DC 表面分子 CD80、CD40和 I-a/e 的表达并增强 CD86的表达及 IL-10的分泌(P <0.05),且一定的剂量效应关系。④结论丙泊酚可能通过介导 IL-10的分泌促进 DC向 CD11clow CD45RBhigh DC 方向分化从而抑制早期炎症反应。

著录项

相似文献

  • 中文文献
  • 外文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号