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柴油机排放颗粒对急性冠状动脉综合征患者外周血单个核细胞白细胞介素1β和肿瘤坏死因子α表达的影响 被引量:2

Effect of diesel exhaust particle on the expression of interleukin-1β and tumor necrosis factor-α in peripheral blood mononuclear cell of acute coronary syndrome patients
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摘要 目的探讨柴油机排放颗粒(DEP)对急性冠状动脉综合征(ACS)患者与非冠状动脉粥样硬化性心脏病(NCHD)患者外周血单个核细胞(PBMC)、白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)表达的影响。方法采用密度梯度离心法分离ACS和NCHD患者PBMC,用不同浓度的DEP(0、10、50、100 mg·L-1)刺激PBMC 24 h。收集PBMC培养液上清,用酶联免疫吸附试验法检测PBMC培养液上清中IL-1β和TNF-α水平。结果随着DEP浓度的增加,PBMC释放IL-1β和TNF-α的量也随之增高,其中以50 mg·L-1组水平最高(P<0.05);在同一DEP浓度下,ACS患者PBMC中IL-1β和TNF-α的相对增加量较NCHD患者高,提示ACS对DEP毒性作用易感。结论 DEP刺激可增加受试患者尤其是ACS患者的PBMC产生过量炎性因子。 Objective To investigate the effect of diesel exhaust particles( DEP) on the expression of including interleukin-1β( IL-1β) and tumor necrosis factor-α( TNF-α) in peripheral blood monocytic cells( PBMC) of acute coronary syndrome( ACS) and non-coronary heart disease( NCHD) patients. Methods The PBMC from ACS and NCHD patients were purified through density gradient centrifugation. The PBMC were incubated with different concentrations of DEP( 0,10,50,100 mg·L- 1) for 24 h. The supernatants were collected and the IL-1β and TNF-α were measured by enzyme-linked immunosorbent assay. Results With increasing of DEP concentration,the IL-1β and TNF-α expressions in PBMCs were increased,which peaked at the dose of 50 mg·L- 1( P〈0. 05). At the same concentration,DEP could induce more production of IL-1βand TNF-α in the PBMCs from ACS patients than that from the NCHD patients,it implied that ACS patients were more susceptible to DEP stimulation. Conclusion DEP stimulation increases the over expression of IL-1β and TNF-α in the PBMCs from the ACS and NCHD patients,especially the former.
出处 《新乡医学院学报》 CAS 2016年第4期288-290,296,共4页 Journal of Xinxiang Medical University
基金 国家自然科学基金面上项目(编号:81573112 81373030) 河南省教育厅科技创新团队项目(编号:14IRTSTHN017) 新乡医学院研究生科研创新支持计划(编号:YJSCX20446Y)
关键词 空气污染 柴油机排放颗粒 外周血单个核细胞 白细胞介素-1Β 肿瘤坏死因子-α 急性冠状动脉综合征 air pollution diesel exhaust particles peripheral blood monocytic cells interleukin-1β tumor necrosis fac tor-α acute coronary syndrome
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