基础医学与临床 ›› 2014, Vol. 34 ›› Issue (5): 690-694.

• 研究论文 • 上一篇    下一篇

紫花前胡苷抑制哮喘小鼠气道炎性反应和NF-κB信号传导通路

熊友谊,时维静,俞浩,张孝林   

  1. 安徽科技学院
  • 收稿日期:2013-11-21 修回日期:2014-01-15 出版日期:2014-05-05 发布日期:2014-04-28
  • 通讯作者: 熊友谊 E-mail:xyytc1@163.com

Inhibitory Effects of Nodakenin on the Airway Inflammation and NF- κB Signaling Pathway in a Murine Asthmatic Model

  • Received:2013-11-21 Revised:2014-01-15 Online:2014-05-05 Published:2014-04-28
  • Contact: You-Yi Xiong E-mail:xyytc1@163.com

摘要: 目的 观察紫花前胡苷抗过敏性哮喘鼠气道炎性反应作用。方法BALB/c小鼠被随机分为对照、模型、紫花前胡苷和地塞米松4组。除对照组外,所有小鼠腹腔注射和雾化吸入卵清蛋白以致敏和诱导气道炎性反应。于每次雾化前1h,给紫花前胡苷组灌胃10 mg/kg紫花前胡苷;给地塞米松组腹腔注射1mg/kg地塞米松。动物肺功能仪分析气道高反应性;细胞计数器和Diff-Quick染色计数支气管灌洗液中白细胞总数及分类;酶联免疫吸附法检测血清或BALF中炎性介质的水平;苏木精-伊红染色法观察气道病理改变;电泳迁移率和免疫印迹法检测肺组织NF-κВ信号通路中蛋白的活力和表达。结果 与对照组比较,模型组呈现明显的气道炎性反应,气道反应性显著增高 (P<0.05);血清或BALF中IgE、IL-4、IL-5和IL-13的水平显著增加 (P<0.01);细胞核P65、p-P65的水平显著增加(P<0.05);细胞质P65和IκBα显著减少,NF-κB DNA-结合力显著增加 (P<0.05)。与模型组比较,紫花前胡苷能够显著抑制气道炎性反应和气道高反应 (P<0.05);降低血清或BALF中IgE、IL-4、IL-5和IL-13的水平 (P<0.01);抑制细胞核P65、p-P65水平 (P<0.05);增加细胞质P65、IκBα蛋白和减弱NF-κB DNA-结合力 (P<0.05)。结论 紫花前胡苷具有抗过敏性哮喘鼠气道炎性反应。

关键词: 紫花前胡苷, 紫花前胡, 哮喘, 核因子κB

Abstract: Objective To observe the effects of nodakenin on airway inflammation in a mouse model of allergic asthma. Methods BALB/c mice were assigned randomly to one of the following four experimental groups: control, model, nodakenin and dexamethasone. All mice, except for those in control group, were sensitized and challenged by OVA to induce airway inflammation. One hour before every OVA challenge, nodakenin group was administered intragastrically with nodakenin at a dose of 10 mg/kg, and dexamethasone group was injected intraperitoneally with dexamethasone a dose of 1 mg/kg. Airway responsiveness was measured by a lung function analysis systems. The number of total leukocytes in BALF was counted using a hemocytometer, and differential cells were counted using Diff-Quick-stained smears. Histopathology of lung tissue was analyzed by Hematoxylin-eosin staining. Levels of inflammatory mediators in serum or BALFs were measured by ELISA. The activity and expression of proteins in NF- κB signaling pathway was respectively evaluated by EMSA and western blot analysis. Results Compared with control group, the model group exhibited obvious airway inflammation, airway reactivity were significantly increased, the levels of total cells and differential cells were significantly increased, levels of IL-4, IL-5, IL-13, IgE were significantly increased, levels of nuclear p65 and p-p65 protein was significantly enhanced, levels of cytoplasmic p65 and IκBα protein were significantly decreased, and the NF-κB DNA binding activity was significantly increased. Compared with model group, nodakenin significantly suppressed airway inflammation, airway hyperreactivity, reduced levels of IL-4, IL-5 and IL-13 in BALF, and IgE in serum, decreased levels of nuclear p65 and p-p65 protein, increased cytoplasmic p65 and IκBα protein, and increased the NF-κB DNA binding activity. Conclusion Nodakenin efficiently inhibited antigen-induced airway inflammation in asthmatic mouse.

Key words: Nodakenin, Peucedanum decursivum Maxim, asthma, NF-κB

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