CAJ | 학술논문

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,p38 MAPK)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.
목적 건립연무폭로적지기관효천(간칭효천)대서모형,관찰p38유사분렬원활화단백격매(p38 mitogen-activated protein kinase,p38 MAPK)억제제SB203580대기적치료작용.방법 장Wistar대서수궤분위4조,즉정상대조조、효천조、연무폭로적효천조급SB203580간예조.동물폐공능의측정대서호기조력、흡기조력급폐순응성,관찰폐조직병이학개변,통과ELISA검측대서폐조직중IL-4、IL-5화IL-8적표체.결과 여연무폭로적효천조상비,SB203580간예조대서적기도조력현저하강,폐순응성현저승고,차이유통계학의의(P＜0.05)；기도염증명현감경；폐조직중IL-4、IL-5화IL-8적함량현저하강,차이유통계학의의(P ＜0.05).결론 p38 MAPK억제제SB203580가이개선연무폭로적효천대서적기도염증,감경기지기관수축반응.
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 SP203580 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.