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作 者:黄静[1] 沈庆[1] 黄方[1] 邬海桥[1] 陈霞[1] 文秀芳[1] 傅燕鸿[1]
机构地区:[1]重庆市第三人民医院呼吸内科,重庆400014
出 处:《中国呼吸与危重监护杂志》2007年第5期369-372,I0002,共5页Chinese Journal of Respiratory and Critical Care Medicine
基 金:重庆市卫生局科研课题(编号:05-2-261)
摘 要:目的探讨气道黏液高分泌与Thl/Th2平衡的关系,以及地塞米松(Dex)对哮喘大鼠气道黏液高分泌及杯状细胞表达的影响。方法30只大鼠随机分为对照组、哮喘组和Dex组,每组10只。哮喘组和Dex组以卵白蛋白激发制作大鼠哮喘模型,Dex组腹腔内注入Dex作为干预因素。分别以HE、阿辛兰染色观察气道上皮的改变、杯状细胞的表达及黏液生成,ELISA法检测血清及支气管肺泡灌洗液(BALF)白细胞介素13(IL-13)和γ干扰素(IFN-γ)的浓度。结果哮喘组较对照组气道上皮杯状细胞数量明显增加(P<0.05),黏液生成增多(P<0.05),血清及BALF中IL-13表达水平显著增高(P均<0.05),IFN-γ表达水平降低(P均<0.05)。Dex组较哮喘组杯状细胞数量显著减少(P<0.05),黏液分泌减少(P<0.05),血清及BALF中IL-13表达水平明显降低(P均<0.05),IFN-γ表达水平升高(P<0.05)。结论Th2型细胞因子IL-13在哮喘大鼠气道上皮杯状细胞化生和黏液高分泌中发挥了重要作用,而Dex可以通过抑制IL-13的表达而减少气道黏液分泌。Objective To observe the effects of dexamethasone(Dex) on Th1/Th2 balance and mucus hypersecrefion in asthmatic mrs. Methods Thirty mrs were randomly divided into 3 groups ( n = 10 in each group), ie. a normal group, an asthma group, and a Dex-treated group. Asthmatic rats were challenged with ovalbumin(OVA). The levels of interleukin-13 (IL-13) and interferon-ganana (IFN-γ) in serum and bonchoalveolar lavage fluid(BALF) were measured by ELISA method. Histochemieal analysis and Aleian blue staining were performed to observe goblet cells and mucus expression. Results Alcian blue staining revealed more mucus and goblet cells in the bronchial epithelial of the asthmatic rats compared to the control rats( P 〈 0.05). Meanwhile, Dex significantly suppressed the production of mucus and hyperplasia of global cells of the asthmatic rats. There was a distinct imbalance of Th1/Th2 in the asthmatic rats. The productions of IL- 13 both in serum and BALF in the asthmatic rats were increased significantly compared to the control mrs( P 〈 0.05), and IFN-γ production in BALI: was lowered remarkably ( P 〈 0.05 ). Dex treatment significantly reduced the production of IL-13 in both serum and BALF( P 〈 0.05),and upregulated the IFN-γ production. Conlusion Dexamethasone can significantly suppresse the mucus hypersecretion and global cells hyperplasia in asthmatic rats by correcting imbalance of Th1/Th2, especially reducing the production of IL-13.
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