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作 者:刘少滨[1] 欧阳金生[2] 黄绍光[3] 万欢英[3]
机构地区:[1]福建医科大学福建省老年医院呼吸内科,福州 350003 [2]温州医学院附属第一医院呼吸内科,温州 325000 [3]上海交通大学医学院瑞金医院呼吸科,上海 200025
出 处:《上海交通大学学报(医学版)》2008年第3期307-309,共3页Journal of Shanghai Jiao tong University:Medical Science
摘 要:目的研究脂多糖-香烟烟雾诱导大鼠水通道蛋白5(AQP5)的表达,以及氨溴索(AMB)对其表达的影响。方法21只SD大鼠随机分为AMB干预组、模型组(脂多糖-香烟烟雾诱导组)与对照组。应用ELISA法检测肺组织匀浆、支气管肺泡灌洗液(BALF)和血清中的TNF-α,原位杂交、免疫组化及图像分析法观察并测定各组AQP5的表达水平。结果模型组肺组织匀浆和BALF中的TNF-α显著高于AMB干预组和对照组(P<0.01);模型组支气管上皮AQP5 mRNA与AQP5蛋白的表达水平低于AMB干预组和对照组(P<0.01);BALF中的TNF-α与AQP5 mRNA和AQP5蛋白的表达呈负相关。结论脂多糖-香烟烟雾可降低支气管上皮AQP5的表达;AMB可能通过抑制BALF中的TNF-α释放而上调AQP5的表达。Objective To investigate the expression of aquaporin-5 (AQP5) in lipo-polysaccharide (LPS)-cigarette smoking inducible SD rats,and the effect of ambroxol chloride (AMB)on its expression. Methods Twenty-one SD rats were randomly divided into three groups: AMB intervention group, model group (LPS-cigarette smoking induction group) and control group. TNF-α was determined from lung homogenate supernatant, bronchial alveolar lavage fluid (BALF) and serum by ELISA. The semi-quantitation of AQP5 transcription and expression were measured by in situ hybridization and immunohistochemistry, respectively. Results TNF-α from lung homogenate supernatant and BALF in model group was more than AMB intervention group and control group ( P 〈 0.01 ). The level of AQP5 mRNA and protein expression in bronchial epithelia in model group were lower than AMB intervention group and control group(P 〈0.01). TNF-α of BALF was negatively correlated with AQP5 mRNA and protein. Conclusion Expression of AQP5 in bronchial epithelia may be decreased by LPS and cigarette smoking. AQP5 expression in bronchial epithelia may be enhanced by AMB through inhibiting the release of TNF in BALF.
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