桑麻杏贝汤对慢性阻塞性肺疾病模型大鼠炎症因子及肺功能作用机制研究

Mechanism of Sangma Xingbei decoction in intervention of inflammatory factors and pulmonary function in rats with chronic obstructive pulmonary disease

目的:探讨桑麻杏贝汤对慢性阻塞性肺疾病(COPD)模型大鼠炎症因子的影响及肺功能的改善作用。方法:将36只SPF级SD大鼠随机分为对照组、模型组和治疗组,每组各12只(雌雄各半),除对照组外,其余两组应用烟熏法构建COPD大鼠模型。治疗组予桑麻杏贝汤12 g/(kg·d)灌胃,模型组和对照组采用10 ml/(kg·d)0.9%氯化钠溶液灌胃。14 d干预结束后,测定大鼠用力肺活量(FVC)、0.1 s用力呼气容积(FEV0.1)、呼气峰值流速(PEF),采用酶联免疫吸附法检测大鼠血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)的浓度水平,并应用HE染色法观察大鼠肺组织病理学变化。结果:与对照组相比,COPD模型组大鼠的FVC、PEF值均下降(P<0.05),血清TNF-α、IL-6、IL-8浓度水平均升高(P<0.01),肺组织病理变化加重。与模型组相比,桑麻杏贝汤组大鼠肺功能明显得到改善(P<0.05),血清炎症因子水平明显降低(P<0.05)。结论:桑麻杏贝汤能够改善COPD模型大鼠的肺功能等症状,其机制可能与下调TNF-α、IL-6、IL-8等炎症因子浓度水平,减少肺组织病理损伤密切相关。

Objective:To explore the effects of Sangma Xingbei decoction on inflammatory factors and pulmonary function and in rats with chronic obstructive pulmonary disease(COPD).Methods:A total of 36 SPF SD rats were divided into normal group,model group and treatment group randomly,with 12 rats in each group(half of male and half of female).Except for the normal group,the other two groups were used to construct COPD model by using cigarette smoke method.The treatment group was given 12 g/(kg·d)of Sangma Xingbei decoction by gavage,and the model group and normal group were given 10 ml/(kg·d)physiological saline by gavage.After 14 days’intervention,the pulmonary function(FVC,FEV0.1,PEF)of the rats was measured,the concentration levels of TNF-α,IL-6 and IL-8 in serum were detected by ELISA and the pathological changes of lung tissue were observed by HE staining.Results:Compared with the normal group,the pulmonary function of model group decreased(P<0.05),and the inflammatory factors(TNF-α,IL-6,and IL-8)increased(P<0.01).The pathological changes of lung tissue were significant.Compared with the model group,the pulmonary function of model group increased(P<0.05),and the inflammatory factors(TNF-α,IL-6,and IL-8)decreased(P<0.05).Conclusion:Sangma Xingbei decoction can effectively improve pulmonary function and its mechanism may be related to down-regulating the concentration levels of inflammatory factors such as TNF-α,IL-6,and IL-8 and preventing the lung tissue from being further destroyed.