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作 者:周晓燕[1] 张力[1] 吴萍[1] 熊维[1] 李咏生[1] 叶笃筠[1]
机构地区:[1]华中科技大学同济医学院基础医学院病理生理学系,武汉430030
出 处:《华中科技大学学报(医学版)》2007年第3期285-288,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:国家自然科学基金资助项目(No.30570726)
摘 要:目的研究脂氧素A4(LXA4)对RAW264.7巨噬细胞免疫功能的影响。方法体外培养小鼠RAW264.7巨噬细胞,分为空白对照组、脂多糖(LPS)组和LXA4组。各组处理预设时间后,RT-PCR检测PIR-A和PIR-B基因表达水平,总一氧化氮检测试剂盒检测一氧化氮含量,流式细胞仪检测细胞表面MHC-Ⅱ分子、CD80(B7-1)、CD86(B7-2)的表达量。结果LXA4显著上调PIR-B,而几乎不影响PIR-A的基因表达水平;明显促进一氧化氮分泌(P<0.01);抑制LPS活化巨噬细胞表达MHC-Ⅱ和CD86(P<0.05),但对CD80的表达无明显影响(P>0.05)。结论LXA4促进巨噬细胞表达免疫抑制分子PIR-B和一氧化氮,抑制巨噬细胞的抗原提呈能力。Objective To investigate the effects of lipoxinon immunodepression molecules and costimulatory molecules in RAW264.7 cells. Methods RAW264.7 cells were treated with lipopolysaccharide (LPS) in the absence or presence of lipoxin A4 for predicted time in vitro. RT-PCR was used to detect the gene expression levels of paired Ig-like receptor (PIR)-B and PIR-A. The supernatants were collected for measuring total NO concentrations by Griess reagent. Flow cytometry was used to determine the expression levels of costimulatory molecules (CD80 [BT-1], CD86 [B7-2]). Results Lipoxin A4 significantly upregulated the gene expression levels of PIR-B, induced the secretion of NO (P〈0.01) and suppressed the expression of MHC- Ⅱ and CD86 (P〈0.05). Conclusion Lipoxin A4 could increase the expression levels of immunodepression molecules PIR-B and NO, but suppress the ability of antigen presenting in RAW264.7 macrophages.
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