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作 者:王再兴[1] 熊慧玲[1] 汪丽云[1] 叶红[1] 余上兵[1] 叶仕桥[1] 王迪浔[1]
机构地区:[1]华中科技大学同济医学院病理生理系卫生部呼吸系疾病重点实验室,湖北武汉430030
出 处:《基础医学与临床》2006年第7期715-719,共5页Basic and Clinical Medicine
基 金:国家自然科学基金(39770309)
摘 要:目的观察雾化吸入地塞米松对吸烟大鼠气道的反应性及支气管平滑肌高电导的钙激活的钾通道(BKca)蛋白和mRNA表达的影响。方法复制大鼠吸烟模型后雾化吸入地塞米松治疗,测定气道反应性;采用HE染色,免疫组织化学染色和原位杂交等方法检测肺组织病理形态学改变和BKca的表达。结果①吸烟组的气道反应性明显高于正常对照组(P<0.05),而吸烟加雾化吸入地塞米松治疗组的气道反应性显著低于吸烟组(P<0.05),但仍高于正常对照组;②吸烟组肺组织出现较轻的炎症反应,吸烟加雾化吸入地塞米松治疗组无炎症反应;③吸烟组大气道和小气道BKcamRNA和蛋白表达低于正常对照组,吸烟加雾化吸入地塞米松治疗组BKcamRNA表达高于吸烟组。结论吸烟引起的气道反应性的增高与气道的炎症反应不平行,雾化吸入地塞米松治疗可降低吸烟引起的气道高反应性,其机制之一可能是降低吸烟对大鼠气道平滑肌BKca表达的抑制作用。Objective To investigate the effect of dexamethasone inhalation on cigarette smoking induced airway hyperresponsiveness and the alteration of potassium channel BKca expression in airway smooth muscle cells. Methods The rat as cigarette smoking model were treated with dexamethasone inhalation, to detect the pathological alteration of rat lung tissue was examined by HE staining, mRNA and protein expression of BKca were determined with in-situ hybridization and immuno-histochemistry techniques. Results (1)Cigarette smoking increased airway responsiveness, the airway responsiveness of dexamethasone treating group lower that of smoking group ( P 〈 0. 05 ), but higher than that of normal control group; (2) HE staining showed, that there was slight pulmonary inflammatory response in cigarette smoking group, no pulmonary inflammatory response in dexamethasone treating group; (3) The protein and mRNA expression of BKca in cigarette smoking group was less than that in normal control group in BSMC of both Bronchioli and Bronchi, dexamethasone treating lead to increase of the protein and mRNA expression of BKca in contrast to cigarette smoking group. Conclusions Cigarette smoking induced increase of airway responsiveness isn't parallel with pulmonary inflammatory response, dexamethasone inhalation can decrease cigarette smoking induced airway hyperresponsiveness, partly resulting from inhibition of potassium channel BKca expression in airway smooth muscle cells induced by cigarette smoking.
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