摘要
目的:探讨LPS诱导的炎症小鼠子宫巨噬细胞迁移和功能活性的调节因素。方法:将150只雌性昆明种小鼠随机分为对照组(A组)、LPS模型组(B组)、MCP-1阻断组(C组),于末次注射后的1、3、6、12、24 h取子宫。运用免疫组织化学方法检测CD14^+巨噬细胞数量与CD14表达的变化,ELISA方法检测TNF-α、MCP-1的表达量。结果:(1)与A组相比,B组内膜、肌层、外膜的CD14^+巨噬细胞数目及CD14表达量在各时间点均极显著增加(P<0.01),C组内膜和肌层在1、3、6 h时恢复至正常水平;与B组相比,C组外膜在1、3、6 h时以及C组的内膜和肌层在各时间点时CD14^+巨噬细胞数目及CD14表达量均极显著减少(P<0.01)。(2)与A组相比,B组在各时间点以及C组在12、24 h时TNF-α和MCP-1的含量极显著增多(P<0.01);与B组相比,C组各时间点的TNF-α和MCP-1的含量极显著减少(P<0.01)。结论:LPS诱导的小鼠子宫炎症反应中巨噬细胞的迁移及CD14、TNF-α等关键分子的表达均受MCP-1的调节。
Objective :To explore the adjustment factors to the migration and functional activity on macrophages in the uterine of inflammatory mice induced by LPS. Methods: 150 Kunming female mouse were divided into control group (group A), LPS model group (group B), MCP-1 blocking-up group (group C), the mice uterines were extracted separately at hour 1,3,6,12,24. The number of CD14 macrophages and the expression of CD14 macrophages were detected by Immunohistochemistry, ELISA detects the expression of TNF-a and MCP-1. Results: @ Compared with group A, the number of CD14 macrophages and the expression of CD14 in endometrium, myometrium, perimrtrium of group B were highly significantly increased ( P 〈 0. 01 ) at every time points, the endometrium,myometrium of group C were closely to normal level at 1,3,6 h; compared with group B, the number of CD14 macrophages and the expression of CD14 were highly significantly decreased(P〈0. 01 )at 1,3,6 h of perimrtrium of group C and every time points of endometrium, myometrium of group C. @Compared with group A, the content of TNF-ct and MCP-1 were highly significantly increased (P〈0. 01 ) at every time points of group B and 12,24 h of group C;compared with group B, the content of TNF-ct and MCP-1 of group C were highly significantly decreased (P〈0. 01 ) at every time points. Conclusion:The migration of macrophages and the expression of CD14 and TNF-a in the uterine of inflammatory mice induced by LPS were rezulated bv MCP-1.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2017年第4期507-510,共4页
Chinese Journal of Immunology
基金
河南省科技攻关项目(No.0524420040)
河南省动物学省级重点学科基金资助