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作 者:罗凤鸣[1] 王曾礼[1] 刘小菁[2] 刘春涛[1] 章小红[1] 王文志[1]
机构地区:[1]四川大学华西医院呼吸科 [2]四川大学华西医院内科实验室,成都610041
出 处:《中华内科杂志》2003年第7期466-469,共4页Chinese Journal of Internal Medicine
基 金:国家自然科学基金资助项目 (3 9770 3 40 )
摘 要:目的 观察大鼠哮喘模型Clara细胞及其分泌蛋白 (CCSP)的表达。方法 SD大鼠 2 4只 ,分为哮喘模型组和健康对照组。哮喘模型组大鼠用卵白蛋白 (OVA)致敏激发建立大鼠哮喘模型。用逆转录 聚合酶链反应、斑点免疫印迹、免疫组化及图像分析方法检测 2组大鼠肺组织CCSPmRNA表达、支气管肺泡灌洗液(BALF)中CCSP蛋白水平、细小支气管Clara细胞比率及气道形态学参数。结果 哮喘模型组大鼠OVA激发2周的支气管总管壁面积、内壁面积及平滑肌面积均较健康对照组和哮喘模型组OVA激发 1周时的增加 (P <0 0 1) ,并与CCSP及其mRNA呈负相关 (r分别为 - 0 5 9、- 0 72、- 0 6 5、- 0 6 3、- 0 78及 - 0 73,P <0 0 1)。哮喘模型组大鼠细支气管、终末细支气管及呼吸性细支气管Clara细胞数量减少 (P <0 0 1或 0 0 5 )。哮喘模型组大鼠肺组织CCSPmRNA表达较健康对照组降低 ,BALF中CCSP蛋白含量降低。结论 CCSPmRNA表达降低 ,Clara细胞数量减少。Objective To investigate the mRNA expression of Clara cell secretory protein(CCSP) and the Clara cell number in airways of rat asthma remodel. Methods A rat asthma model was established by sensitization and challenge with ovalbumin (OA). The mRNA expression of CCSP in the lung tissue, the CCSP level in bronchial alveolar lavage fluid (BALF), the thickness of the airways and the number of Clara cells in bronchioles were determined by RT-PCR, image analysis system,dot immunoblotting and immunohistochemistry methods. Results There was a progressive decline in CCSP mRNA expression in the lung tissue of rat asthma model group(0.53±0.07 and 0.49±0.03, respectively ,after 1 week and 2 weeks of challenge)as compared to that of control group(0.67±0.04).The CCSP levels in BALF of asthma model group(47.00±6.58 and 45.95±3.20, respectively , after 1 week and 2 weeks of challenge )were significantly decreased than that of control group(63.08±2.84, P <0.01). The ratio(%) of Clara cells was also reduced after challenge. The WAt/Pbm, WAi/Pbm, and WAm/Pbm were significantly increased 2 weeks after OA challenge and were negatively correlated with the level of CCSP and its mRNA expression. Conclusion The Clara cells and CCSP may participate in the pathogenesis of asthma in the rat asthma remodel.
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