目的:探讨白花蛇舌草对哮喘小鼠气道炎症的治疗作用及其作用机制。方法:把40只清洁级BABL/c小鼠,随机数字表法分为4组,每组10只,分别为生理盐水对照组、哮喘模型组、白花蛇舌草组、糖皮质激素组。在末次激发24 h后所有小鼠取左肺组织行HE染色和PAS染色,观察哮喘组肺组织炎症浸润和结构破坏情况。用酶联免疫吸附法(ELISA)观察小鼠支气管肺泡灌洗液(BALF)中细胞的总数和各种炎症细胞计数的变化以及白细胞介素-4(Interleukin 4,IL-4)、白细胞介素-5(Interleukin5,IL-5)、白细胞介素13(Interleukin13,IL-13)及干扰素-γ(Interferon-gamma,IFN-γ)含量;取右肺组织用Westernblot检测NF-κB p65的表达变化情况。结果:哮喘模型组小鼠与对照组相比较,BALF中的嗜酸粒细胞计数及IL-4、IL-5、IL-13水平均出现增高,而IFN-γ水平出现降低,且肺组织中的NF-κB p65表达水平显著高于对照组(P〈0.05);白花蛇舌草组和糖皮质激素组小鼠与哮喘组小鼠相比炎症细胞计数、IL-4、IL-5、IL-13以及NF-κB p65表达水平均显著降低而IFN-γ水平则明显上升,且具有显著性差异(P〈0.05)。结论:白花蛇舌草通过阻断NF-κB p65表达,下调哮喘小鼠BALF中IL-4、IL-5、IL-13水平,同时上调BALF中IFN-γ水平以及降低炎症细胞数量,从而抑制气道炎症。
OBJECTIVE To study the effect and mechanism of action of Hedyotis diffusa water extract (HDWE) on airway inflammation and remodeling in mice model with asthma. METHODS 40 Male BALB/c mice models of asthma were randomly divided into 4 groups: asthma group, control group, HDWE group,dexamethasone group. All mice were killed 24 h after final OVA challenge. The left lung was isolated for pathological examination. Lung sections were stained with hematoxylin and eosin (HE), Masson'S trichrome. The thickness of bronchial airway, bronchial smooth muscle thickness, and the collagen deposi- tion area were measured by image analysis system. The concentrations of IL-4, IL-5, IL-/3 and IFN-γin BALF were measured by ELISA, the Western blot was performed to detect NF-~B p65 from the right lung tissues. RESULTS In asthma group, the number of inflammatory cells and the expression of IL-4, IL-5, IL-13 in BALF was higher than the control group, IFN-7 was lower;NF-~B p65 in lung was significantly higher than those in control group (P〈0. 05). HDWE group and dexamethasone group significantly decreased. The number of inflammatory cells, the expression of IL-4,IL-5, ILl3 in BALF, the content of NF-κB p65 in lung tissues were significantly lower, but IFN T was higher, with differences (P〈0.05). CONCLUSION The hedyotis diffusa inhibits the expression of NF-κeB p65, rerduce the level of IL-4, IL-5, IL-13, and increases the level of IFN-γin asthmatic model to inhibit asthma attack and airway inflammation. KEY WORDS.. asthma; Hedyotis diffusa; NF-κB p65