荜茇对哮喘模型小鼠Th1/Th2细胞因子的影响

Effects of the Piperis Longi Fructus on cytokines level of type Th1/Th2 in mice model with asthma

目的:探讨荜茇乙醇提取物对哮喘小鼠气道炎症的治疗作用及其作用机制。方法:40只清洁级BABL/c小鼠按随机数字表法分为4组,分别为生理盐水对照组、哮喘模型组、荜茇乙醇提取物低和高剂量组(100 mg/kg、200 mg/kg)。在末次激发24 h后所有小鼠取左肺组织行HE染色,观察哮喘组肺组织炎症浸润情况。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(IL-4)、IL-5及干扰素-γ(IFN-γ)含量;取右肺组织用Westernblot检测NF-kB p65蛋白的表达情况。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、IL-4、IL-5水平增高和IFN-γ水平降低,肺组织中的NF-kB p65表达水平显著高于对照组;荜茇乙醇提取物低剂量组(100 mg/kg)和高剂量组(200 mg/kg)小鼠与哮喘组小鼠相比炎症细胞计数、IL-4、IL-5以及NF-kB p65蛋白表达水平均显著降低而IFN-γ水平明显上升,具有显著的差异。结论:荜茇乙醇提取物在体内可能主要通过NF-kB p65等转录因子调节Th2反应。

The effect and mechanism of action of effect of ethanol extract from Pipefis Longi Fructus（EEPL） to asthma mice airway in- flammation and remodeling. Methods： 1. Preparations for the models of the asthma mouse 40 Male BALB/c mice, were randomly divided into 4 groups, and the groups were asthma group, contral group, EEPL low-dose group（ 100 mg/kg）, EEPL high-dose group（200 mg/kg）. All mice were killed 24 h after final OVA challenge. The left lung was isolated for pathological examination. Lung sections were stained with be- matoxylin and eosin （HE）. The thickness of bronchial airway, bronchial smooth muscle thickness, and the collagen deposition area were measured by image analysis system. The concentrations of IL-4,IL-5 and IFN-γin BALF were measured by ELISA, the western blote was performed to detect NF-kB p65 protein from the right lung tissues. Results： In asthma group, the number of inflammatory cells and the ex- pression of IL-4 、IL-5 in BALF is higher than the control group, IFN-γ/were lower; NF-kB p65 in lung is significantly higher than those in control group （P 〈 0.05 ）. EEPL low-dose group （100 mg/kg） ,EEPL high-dose group（200 mg/kg） significantly decreased. The number of inflammatory cells, the expression of IL-4 、IL-Sin BALF, the content of NF-kB p65 proteinin lung tissues were significantly lower, but IFN-T were higher, with differences （P 〈0.05）. Conclusion： EEPL decoction may modulate Thl/Th2 balance by suppressing the gene expression of NF-kB p65 in vivo.