阿司匹林对树突状细胞成熟及免疫功能的体外研究  

Effect of aspirin on maturation and function of murine myeloid dendritic cells in vitro

作　　者：周游[1] 李大主[1] 吴伟[1] 曾秋棠[1] 

机构地区：[1]华中科技大学同济医学院协和医院心内科,武汉430022

出　　处：《现代免疫学》2005年第5期366-369,共4页Current Immunology

基　　金：日本内田国际资助项目(1995年度)

摘　　要：研究阿司匹林在体外对小鼠树突状细胞(mDC)成熟及免疫功能的影响。在骨髓来源未成熟树突状细胞培养过程中,加入不同剂量(1mmol/L、2mmol/L)的阿司匹林,观察DC形态。流式细胞仪检测各组mDC表面共刺激分子CD86、CD80的表达;台盼蓝染色测细胞活力;混合淋巴细胞反应(MLR)检测mDC对T淋巴细胞刺激能力;ELISA法检测MLR上清液中细胞因子。与对照组比,阿司匹林处理的DC(aspirin-DC)表面CD80、CD86表达明显降低(P<0.01);对T淋巴细胞刺激能力减弱;MLR上清液中炎性因子(TNF-α、IL-1β)明显减少(P<0.01)。结果:在体外培养过程中给予阿司匹林干预能够抑制mDC的成熟及功能,呈剂量依赖性;阿司匹林对DC功能的抑制可能是阿司匹林抑制炎症反应,治疗冠心病的机制之一。To study effect of aspirin on the function of murine myeloid dendritic cells in vitro, bone marrow-derived dendritic cells progenitors from C57BL/6J mice were treated with or without. Aspirin and flow cytometric analysis was used to detect the expression of co-stimulating factor CD86, CD80 on DC. The stimulating capacity of DC was determined by allogenic mixed lymphocyte reaction （MLR） and ELISA was used to analyze the level of cytokines in the supernatants of cultures with MLR. Compared with untreated group, CD86, CD80 on DC was significantly less expressed in aspirin-treated DC groups（P〈0.01）, and the stimulating capacity of DC in MLR was lower： T lymphocytes in MLR secreted lower levels of pro-inflammation cytokines （TNF-α and IL-1β）（P〈0.01）, the inhibitory action was dose dependent and was evident at higher concentrations. It concludes that aspirin has suppressive influences on the expression of co-stimulating factor and stimulating capacity of DC, and inhibitory effect of aspirin on inflammation and treatment of aspirin on coronary artery disease may be due to its inhibition on DC.

关 键 词：阿司匹林 树突状细胞 细胞因子 免疫功能 冠心病 

分 类 号：R392.12[医药卫生—免疫学] R543.3[医药卫生—基础医学]