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作 者:李云霞[1] 李男[1] 加慧 夏书月[1] Li Yunxia;Li Nan;Jia Hui;Xia Shuyue(Department of Respiratory Medicine,the Affiliated Central Hospital of Shenyang Medical College,Shenyang 110024,China)
出 处:《国际呼吸杂志》2019年第5期340-344,共5页International Journal of Respiration
基 金:沈阳医学院博士启动基金(20174047);辽宁省自然科学基金面上项目(20170540865).
摘 要:目的研究miR-155在慢性阻塞性肺疾病(COPD)患者中的表达水平及其与炎性细胞因子的相关性。方法选取2017年6月至2018年6月在沈阳医学院附属中心医院呼吸科门诊就诊的稳定期COPD患者30例,住院的COPD急性加重期(AECOPD)患者30例,重度吸烟组30例,健康对照组30例。抽取各组患者外周血,逆转录聚合酶链反应(RT-PCR)检测单个核细胞(PBMC)中miR-155的表达水平;酶联免疫吸附试验(ELISA)方法检测肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、IL-1β、IL-17细胞因子水平;分析各组指标之间的相关性。结果AECOPD组miR-155表达量最大,COPD稳定组表达量次之,重度吸烟组表达量较少,健康对照组表达量最少。对miR-155与上述炎症因子的表达进行相关分析,结果显示miR-155与上述指标均存在正向相关(r=0.971、0.949、0.963、0.975),差异具有统计学意义(P<0.01)。结论miR-155可能参与COPD的炎症反应,促进COPD的发生、发展。Objective To study the expression level of miR-155 in patients with chronic obstructive pulmonary disease(COPD) and its correlation with inflammatory cytokines.Methods Thirty patients with stable COPD who were admitted to the respiratory department of our hospital from June 2017 to June 2018 were enrolled.30 patients with acute exacerbations of COPD were hospitalized(AECOPD group),30 patients with severe smoking,and 30 healthy controls.Peripheral blood of each group was taken out,and the expression level of miR-155 in PBMC of mononuclear cells was detected by reverse transcription polmerase chain reaction (RT-PCR).The levels of tumor necrosis factor a(TNF-a),interleukin 6(IL-6),IL-1β and IL-17 cytokines were detected by ELISA.Analyze the correlation between the various groups of indicators.Results The expression of miR-155 was the highest in the AECOPD group,followed by the COPD stable group.The expression in the severe smoking group was less,and the healthy control group had the least expression.Correlation analysis between miR-155 and the expression of the above inflammatory factors showed that miR-155 was positively correlated with the above indicators(r=0.971,0.949,0.963,0.975),and was statistically siguificant(P<0.01).Cuuclusiuns liR-155 may be involved in the inflammatory response of COPD and promote the development of COPD.The specific pathways and mechanisms need further study.
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