Expression of NOD1 and NOD2 mRNA in peripheral dendritic cell in patients with acute coronary syndrome
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摘要: 目的:探讨寡聚结构域1 (nucleotide-binding oligomerization domain, NOD)和NOD2在急性冠状动脉综合征(ACS)患者树突状细胞中表达水平及意义。方法:研究纳入58例患者,包括16例ST段抬高型心肌梗死(STEMI)患者、20例不稳定心绞痛患者(UAP)和12例稳定型心绞痛患者(SAP),及10例健康体检者作正常对照组(CTRL)。由外周血单个核细胞经含粒细胞巨噬细胞集落刺激因子和白细胞介素(IL)4培养获得树突状细胞。用实时荧光定量聚合酶链反应(RT-PCR)检测树突状细胞NOD1及NOD2 mRNA表达水平,流式细胞仪分析各组DC表面分子,ELISA检测外周血IL-8和C反应蛋白浓度,分析NOD1和NOD2 mRNA与CD80、CD86表达的相关性。结果:与SAP及CTRL组比较,STEMI及UAP组外周血IL-8和C反应蛋白浓度增加,DC细胞共刺激分子CD80、CD86表达明显上调,其胞内NOD2 mRNA表达水平增加,而NOD1水平无显著差异;NOD2 mRNA表达水平与树突状细胞CD80、CD86表达呈显著相关。结论:NOD途径可能参与了动脉粥样硬化的发生发展;树突状细胞可能通过NOD2途径在促动脉粥样斑块不稳定的炎症反应中发挥重要作用。Abstract: Objective: To explore the level of NOD1 and NOD2 mRNA expression in peripheral dendritic cell(DC) in patients with acute coronary syndrome(ACS). Method: The 58 patients, consisted of 16 patients with ST-segment elevation myocardial infarction(STEMI), 20 patients with unstable angina pectoris(UAP), 12 patients with stable angina pectoris(SAP) and 10 control(CTRL) healthy subjects were admitted. DCs derived from peripheral blood monocytes were isolated and cultured in vitro with rhGM-CSF and rh IL-4.RT-PCR was used to analyze the expression of NOD1 and NOD2 mRNA in DCs. The flow cytometric analysis was used to detect the expression of co-stimulating factors(CD80, CD86, HLA-DR) on DCs. ELISA was used to analyze the level of cytokines IL-8 and C-reactive protein(CRP) in blood. Relationship between NOD1 or NOD2 mRNA level and co-stimulating factors was also analyzed. Result: Compared with SAP and CTRL group,much more CD86 and CD80 were expressed on DCs in STEMI and UAP group, NOD2 mRNA was also up-regulated, IL-8 and CRP in peripheral blood of both groups increased. But NOD1 mRNA did not increase relatively. NOD2 mRNA level correlated with CD80 and CD86 expression significantly. Conclusion: NOD-mediated immune pathway may be involved in the pathogenesis of atherosclerosis. DC plays an important role in the inflammation of unstable plaque via NOD2 pathway probably.
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