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作 者:李雯[1,2] 林江涛[2] 孙力超[3] 周童亮[4] 李鸿[4] 潘琳[4] 郭艳茹[4] 张岚[4] 舒峻[4]
机构地区:[1]北京协和医学院研究生院,100730 [2]中日友好医院呼吸内科,北京100000 [3]中日友好医院急诊科,北京100000 [4]中日友好医院临床医学研究所中心实验室,北京100000
出 处:《中华哮喘杂志(电子版)》2012年第6期399-402,共4页Chinese Journal of Asthma(Electronic Version)
摘 要:目的建立烟雾暴露的支气管哮喘(简称哮喘)大鼠模型,观察p38有丝分裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38MAPK)抑制剂SB203580对其的治疗作用。方法将Wistar大鼠随机分为4组,即正常对照组、哮喘组、烟雾暴露的哮喘组及SB203580干预组。动物肺功能仪测定大鼠呼气阻力、吸气阻力及肺顺应性,观察肺组织病理学改变,通过ELISA检测大鼠肺组织中IL-4、IL-5和IL-8的表达。结果与烟雾暴露的哮喘组相比,SB203580干预组大鼠的气道阻力显著下降,肺顺应性显著升高,差异有统计学意义(P<0.05);气道炎症明显减轻;肺组织中IL-4、IL-5和IL-8的含量显著下降,差异有统计学意义(P<0.05)。结论 p38 MAPK抑制剂SB203580可以改善烟雾暴露的哮喘大鼠的气道炎症,减轻其支气管收缩反应。Objective To establish model of cigarette smoke exposure to asthmatic rats and investigate the effect of a p38 mitogen-activated protein kinase(p38 MAPK) inhibitor SB203580 on the model.Methods Wistar rats were randomly divided into four groups:normal group, asthmatic group, cigarette smoke exposure to asthmatic group and SB203580 group. Rat lung function was measured by animal pulmonary function meter. ELISA was used to detect the expression of cytokines in lungs of rats.Results Compared to the cigarette smoke exposure to asthmatic group, the rats of SB203580 group had a lower airway resistance and a higher pulmonary compliance,the difference was statistically significant (P<0.05). SB203580 treatment attenuated airway inflammation. The results of ELISA showed the level of IL-4, IL-5 and IL-8 was lower in SB203580 group than cigarette smoke exposure to asthmatic group.Conclusions It is suggested that p38 MAPK inhibitor SB203580 may be effective on reducing airway inflammation and bronchial contractile response in cigarette smoke exposure to asthmatic rats.
关 键 词:支气管哮喘 糖皮质激素 p38有丝分裂原活化蛋白激酶
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