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通过测定慢性阻塞性肺疾病(Chronic Obstructive Pulmonary Disease,COPD)西北寒燥证模型外周血中炎症因子IL-1β、IL-8、IL-10、TNF-α含量的变化,揭示COPD西北寒燥证模型全身炎症反应状态。利用气管滴注弹性蛋白酶结合熏烟的方法建立COPD模型,在此基础上施以寒燥环境应激以建立COPD西北寒燥证模型。利用酶联免疫吸附测定(Enzyme-Linked Im-munoadsordent Assay,ELISA)法测其外周血血清中IL-1β、IL-8、IL-10、TNF-α含量。结果表明,大鼠血清中弹性蛋白酶加熏烟加寒燥组(酶加CS加寒燥组)的IL-1β含量高于空白对照组(P<0.05);模型组IL-8、IL-10、TNF-α含量较空白对照组虽有增高趋势,但3组均不具有统计学差异。故而认为,西北寒燥证(寒燥)引起的全身炎症反应主要以增加血清中IL-1β含量为主,提示西北寒燥证具有加重COPD全身炎症的趋势,方域特色COPD的治疗应引起重视;西北寒燥证参与了COPD的发病,但其不是COPD中较重的证型,应尽早对其加以调控和预防。
The changes of IL-1β, IL-8, IL-10 and TNF-α in peripheral blood of Chronic Obstructive Pulmonary Disease (COPD) Model systemic inflammatory response status. The use of tracheal instillation of elastase combined with fumigation COPD model established on the basis of cold and dry conditions to impose cold to establish COPD northwest cold dryness syndrome model. Serum levels of IL-1β, IL-8, IL-10 and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA). The results showed that the content of IL-1β in the serum of rats with elastase plus fuming and adding dryness group (CS + Hanhan group) was higher than that of the blank control group (P <0.05); IL-8 and IL-10 , TNF-αcontent increased compared with the control group, but there was no statistical difference among the three groups. Therefore, the cold syndrome in the northwest (cold dry) caused systemic inflammatory response mainly to increase serum IL-1β content, suggesting that the northwest cold syndrome has the tendency to aggravate COPD systemic inflammation, the treatment of square characteristics of COPD should pay attention ; Northwest cold syndrome involved in the pathogenesis of COPD, but it is not the COPD heavier card type should be its early regulation and prevention.