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作 者:张丽琴[1] 陈兴无[1] 涂雄文[1] 孙珍贵[1]
机构地区:[1]皖南医学院弋矶山医院呼吸内科,安徽芜湖241001
出 处:《中国实用内科杂志》2010年第8期711-714,共4页Chinese Journal of Practical Internal Medicine
基 金:中华医学会临床医学CRD专项资金资助(07010110019);安徽省教育厅自然科学研究项目(KJ2009B160)
摘 要:目的探讨不同人群对烟雾炎症反应的差异。方法选择2008年1月至2009年4月在皖南医学院弋矶山医院呼吸内科就诊的慢性阻塞性肺疾病(COPD)患者33例,其中吸烟者17例,戒烟者16例。并财时选取"健康"吸烟者13例,不吸烟者9例。计数痰细胞,测量白介素(IL)-8、IL-6,以5%香烟烟雾提取物(CSE)刺激受试者全血或5%CSE刺激预先添加斯伐他汀全血6h,测定上清中IL-8、IL-6及丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢活性(CAT)。结果相对于健康吸烟或不吸烟组,COPD组痰细胞总数及中性粒细胞百分比明显增高,症状评分明显增加(P<0.05)。所有吸烟组痰、血IL-8均比不吸烟组明显高,5%CSE刺激全血IL-8释放,COPD吸烟组更明显,而健康吸烟组最弱(P<0.05)。COPD吸烟组痰、血IL-6浓度明显高于健康吸烟组(P<0.05),5%CSE刺激全血IL-6释放,健康不吸烟组增加最明显。斯伐他汀减弱5%CSE诱导的IL-8、IL-6释放。5%CSE上调全血MDA表达,COPD吸烟组更明显、健康吸烟组最弱(P<0.05)。5%CSE降低GSH-Px水平,其中健康吸烟组降低幅度最小;5%CSE降低COPD组SOD、CAT水平,但健康吸烟组和不吸烟组代偿性增高。斯伐他汀不同程度减弱或抑制CSE的上述效应。结论 COPD吸烟患者较健康吸烟者对香烟烟雾易感性更强,斯伐他汀可有效调节吸烟患者香烟烟雾诱发的血浆炎症反应及氧化/抗氧化状态。Objective To investigate the different inflammatory reaction by smog between smoking populations. Methods COPD smokers, ex-smokers, healthy smokers and nonsmokers were studied. Sputum inflammatory cell counts,interleukin (IL)-8, and IL-6 were evaluated. In supernatant of 5% cigarette smoke extract (CSE) stimulated whole blood or 5 % CSE stimulated whole blood pretreated with simvastatin, levels of IL-8,6, MDA, GSH-Px, and SOD, CAT were measured. Results Compared with healthy smokers and nonsmokers, the number of sputum cells and the percentage of neutrophils were obviously higher and symptom score increased significantly in COPD smokers (P 〈 0. 05 ). IL-8 levels in sputum and blood were significantly higher in smokers compared to nonsmokers. Quantity of IL-8 elicited by 5% CSE in whole blood in COPD smokers was obviously higher than in healthy smokers (P 〈 0. 05 ) , so were levels of IL-6 in sputum and blood (P 〈 0. 05 ) and 5 % CSE induced IL-6 release from blood. Simvastatin attenuated 5% CSE-induced whole blood IL-8, IL-6 release. MDA expression upregulated by 5 % CSE in COPD smokers rised maximum, whereas healthy smokers minimum (P 〈 0. 05 ). GSH-Px levels reduced by 5% CSE in healthy smokers dropped least;SOD, CAT levels were reduced by 5 % CSE in COPD smokers, but compensatory increase in healthy smokers and nonsmokers. Simvastatin reduced or suppressed the above-mentioned effects of CSE to different extent. Conclusion COPD smokers have much more susceptibility to cigarette smoke than healthy smokers, simvastatin can effectively regulate plasma inflammation and oxidative / antioxidant status induced by cigarette smog in smokers.
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