摘要
目的观察胡黄连苷Ⅱ对支气管哮喘(简称哮喘)大鼠气道炎症和支气管收缩的影响。方法将30只Wistar大鼠按随机数字表分成正常对照组(A组)、哮喘模型组(B组)、胡黄连苷Ⅱ干预组(c组),用卵白蛋白系统致敏加局部激发的方法制作哮喘模型,C组第8天起给予胡黄连苷II(100mg/kg)灌胃。第15天给予2oA卵白蛋白液诱喘,观察各组大鼠的诱喘表现、诱喘潜伏期变化。第22天给予气道阻力测定;BALF中细胞计数及分类计数、外周血嗜酸粒细胞(EOS)计数、酶联免疫吸附法测定血清和BALF中Th1/Th2细胞因子IFN-γ、IL-4水平;HE染色病理观察支气管肺组织切片。结果与B组相比,C组大鼠诱喘潜伏期明显延长(t=-5.961,P〈0.01),诱喘反应减轻;基础呼气阻力降低(t=11.014,P〈O.05),肺顺应性升高(t=-2.365,P〈O.05);BALF中细胞总数和E0s计数明显减少(t值分别为16.685、5.519,P〈0.01);外周血EOS计数显著降低(t=13.730,P〈O.01);血清及BAI。F上清中IFN—Jy的水平显著升高(t值分别为-11.589、-9.177,P〈0.01),IL-4的水平显著降低(f值分别为13.728、25.649,P〈O.01);支气管壁炎性细胞浸润减少,支气管壁及血管周围EOS浸润明显减少。结论胡黄连苷Ⅱ对哮喘大鼠具有一定的抑制支气管收缩的作用,并可以抑制哮喘大鼠气道局部炎症反应,改善气道局部和全身的Th亚群失衡。
Objective To observe picroside H effects on airway inflammation and bronchial contraction in a rat asthmatic model. Methods Thirty Wistar rats were randomly divided into three groups:control group (group A, n = 10), asthmatic model group (group B, n = 10), and picroside H treatment group(group C, n: 10). Both group B and group C were sensitized by intraperitoneal injection of OVA and challenged by aerosolized OVA to establish the asthmatic model. Then the following examinations were performed on all rats. Provocation symptom and wheezing-induced delitescence were observed, the pulmonary function was tested, total cell number and differential inflammatory cell number in BALF and E()S number in blood were counted under light microscope^the expressions of Thl cytokine (IFN-y) and Th2 cytokine (IL-4) of BALF and serum were quantified by ELISA technique; and the pathomorphological changes in tile lung tissue stained with HE were observed. Results Compared with group B, group C had a longer wheezing-induced delitescence, a lower expiratory resistance, a higher dynamic lung compliance, and a significant fewer number of WBC and EOS in BALF and in blood, an increased IFN-γ level and a decreased IL-4 level of BALF and serum, an alleviative bronchial inflammation. Conclusions Picroside Ⅱ can inhibit airway inflammation and bronchial contraction in rat asthmatic model, and can regulate the balance of Th2/Th2.
出处
《国际呼吸杂志》
2014年第3期166-169,共4页
International Journal of Respiration