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C1q肿瘤坏死因子相关蛋白3对AMI患者外周血中间型(CD14++CD16+)单核细胞分化的影响及其机制
作者:彭中兴1  陈昊颖1  李琳青1  侯建同1  刘波1  朱红涛3  汤成春2 
单位:1. 东南大学 医学院, 江苏 南京 210009;
2. 东南大学附属中大医院 心内科, 江苏 南京 210009;
3. 丹阳市人民医院 心内科, 江苏 镇江 212300
关键词:C1q肿瘤坏死因子相关蛋白3 中间型(CD14++CD16+)单核细胞 急性心肌梗死 
分类号:R542.22;R-33
出版年·卷·期(页码):2019·38·第二期(242-248)
摘要:

目的:通过C1q肿瘤坏死因子相关蛋白3(CTRP3)对急性心肌梗死(AMI)患者外周血中单核细胞分化过程的研究,探讨CTRP3对中间型(CD14++CD16+)单核细胞功能的影响。方法:采用密度梯度离心法从AMI患者外周血中分离出单核细胞,用台盼蓝染色检测细胞活力。流式细胞仪检测AMI患者外周血中间型(CD14++CD16+)单核细胞的比例。酶联免疫吸附测定和实时聚合酶链反应检测中间型(CD14++CD16+)单核细胞中炎症因子IL-6和TNF-α的表达。结果:(1)AMI患者外周血单核细胞存活率超过90%。(2)CTRP3可诱导AMI患者中间型(CD14++ CD16+)单核细胞的分化(P<0.05)。(3)CTRP3抑制介导的中间型(CD14++CD16+)单核细胞IL-6和TNF-α的表达(P值<0.05)。(4)中间型单核细胞上的ERK1/2和P38-MAPK信号通路参与了脂肪酶介导的炎症活化过程(P<0.05)。结论:干预CTRP3可能成为一种改善AMI患者预后的重要方法。

Objective:To investigate the effect of C1q/TNF-related protein-3(CTRP3) on the function of intermediate type (CD14++CD16+) monocytes by studying the differentiation process of monocytes in peripheral blood of patients with acute myocardial infarction (AMI) under the effect of CTRP3. Methods:In this study, monocytes were isolated from AMI patient's peripheral blood by density gradient centrifugation and their viability was detected by trypan blue staining. Flow cytometer was utilized to detect the proportion of CD14++CD16+ monocytes. The expressions of inflammatory factors IL-6 and TNF-α in CD14++CD16+ monocytes were measured by ELISA and RT-PCR assay. Results:(1) The monocyte viability was more than 90% in peripheral blood of AMI patients. (2) CTRP3 could induce the differentiation of the intermediate type (CD14++CD16+)monocytes from monocytes in peripheral blood of AMI patients(P<0.05). (3) Expressions of inflammatory factors IL-6 and TNF-α induced by LPS were inhibited by CTRP3(P<0.05). (4) LPS-mediated inflammatory activation process was interfered by the ERK1/2 and P38-MAPK signaling pathways(P<0.05). Conclusion:The intervention of CTRP3 may become an important method to improve the prognosis of patients with AMI.

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