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机构地区:[1]河北省廊坊市中医医院西药房,河北廊坊065000 [2]中国石油天然气总公司中心医院药剂科,河北廊坊065000 [3]河北省廊坊市人民医院药剂科,河北廊坊065000
出 处:《实用临床医药杂志》2015年第23期41-43,47,共4页Journal of Clinical Medicine in Practice
基 金:中国高校医学期刊临床专项资金(11522744)
摘 要:目的探讨糖皮质激素对哮喘患者外周血单核细胞Toll样受体4(TLR4)和相关炎症因子表达的影响。方法 50例哮喘急性发作患者设为观察组,接受糖皮质激素治疗,按病情发展分为急性期和缓解期。另选取50名体检健康者为对照组。PCR检测2组外周血单核细胞(PBMCs)TLR4的mRNA和蛋白表达,ELISA法检测PBMCs培养上清白细胞介素-6(IL-6)、IL-8、肿瘤坏死因子?α(TNF?α)表达水平。结果观察组患者急性期PBMCs中TLR4 mRNA含量为(0.039±0.010),高于缓解期的(0.016±0.005)和对照组的(0.014±0.004),差异有统计学意义(P<0.01);观察组急性期和缓解期PBMCs培养上清中TLR4、IL-6、IL-8、TNF?α的水平显著高于对照组(P<0.01);观察在急性期上述指标表达水平显著高于缓解期,(P<0.05或P<0.01)。相关性分析显示,TLR4与IL-6、IL-8、TNF?α之间呈正相关(P<0.01)。结论糖皮质激素治疗通过抑制哮喘患者外周血单核细胞TLR4的表达,而后者可能通过调控IL-6、IL-8、TNF?α等炎症因子表达水平参与哮喘进展过程。Objective To investigate the effects of inhalation of glucocorticoids on expression of peripheral blood mononuclear cell toll-like receptors 4( TLR4) and inflammation-associated cytokines in asthma patients. Methods A Total of 50 acute asthma patients were recruited as observation group and received inhalation of glucocorticoids,another 50 healthy subjects were selected as controls.Expression of protein and mRNA of toll-like receptors 4( TLR4) from peripheral blood mononuclear cell( PBMCs) were detected by PCR methods,and levels of interleukin-6( IL-6) 、IL-8 and tumor necrosis factor?α( TNF?α) were tested by ELISA Methods. Results The TLR4 mRNA content was( 0.039 ± 0. 010) in acute asthma patients,which was higher than that of remission stage( 0. 016 ± 0.005) and controls( 0. 014 ± 0. 004),with significant difference( P〈0. 01). The observation group at acute stage and remission stage had higher levels of TLR4、IL-6、IL-8、TNF?αin PBMCs culture supernatants compared with the controls( P〈0. 01),and was higher in patients at acute stage than those at remission stage( P〈0. 05,P〈0. 01). The level of TLR4 were positive correlated with IL-6、IL-8、TNF?α( P〈0. 01). Conclusion The suppression expression of TLR4 by glucocorticoids treatment is highly relevant to the regulation of inflammation-associated cytokines such as IL-6、IL-8 and TNF?α.
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