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作 者:申永刚 高汇雯 胡昕伟 李汶鸿 何静 张雪飞 王涵 丁圣刚[3] 沈兵 Shen Yonggang;Gao Huiwen;Hu Xinwei;Li Wenhong;He Jing;Zhang Xuefei;Wang Han;Ding Shengang;Shen Bing(Teaching and Research Section of Internal Medicine-Pediatrics,Department of Nursing,Anhui Health College,Chizhou 247099,Anhui,China;Teaching and Research Section of Physiology,School of Basic Medical Sciences,Anhui Medical University,Hefei 230032,Anhui,China;Department of Pediatrics,The First Affiliated Hospital of Anhui Medical University,Hefei 230022,Anhui,China)
机构地区:[1]安徽卫生健康职业学院护理系内儿教研室,安徽池州247099 [2]安徽医科大学基础医学院生理学教研室,安徽合肥230032 [3]安徽医科大学第一附属医院儿科,安徽合肥230022
出 处:《右江民族医学院学报》2022年第1期25-28,共4页Journal of Youjiang Medical University for Nationalities
基 金:安徽省教育厅重点项目(KJ2018A0974)。
摘 要:目的 探讨哮喘大鼠的气管平滑肌细胞中瞬时受体电位多囊蛋白2(TRPP2)的改变及其在气管收缩中的病理作用。方法 随机将大鼠分为对照组和哮喘模型组。将新配制的致敏液腹腔注射制备哮喘动物模型,于第1天和第8天进行腹腔注射,在第15~20天时采用1%OVA雾化吸入进行致敏;对照组中,致敏液替换为磷酸盐缓冲溶液。采用气管张力实验观察钙库操纵的钙内流(SOCE)引起的气管平滑肌收缩中的改变;采用TRPP2siRNA转染敲低TRPP2;TRPP2蛋白表达采用Western Blot和免疫组化进行观察。结果 成功复刻哮喘模型后,哮喘组SOCE引起的气管收缩在高钾引起的收缩中占比明显高于对照组(P <0.05);TRPP2蛋白在哮喘组大鼠气管平滑肌细胞中表达水平升高(P<0.05)。使用TRPP2siRNA敲低TRPP2含量,与对照大鼠气管相比,SOCE引起的TRPP2敲低后的大鼠气管收缩在高钾引起收缩百分比中显著减小(P <0.05)。结论 哮喘大鼠气管平滑肌中表达上调的TRPP2可能是导致SOCE引起的收缩增强的主要原因。Objective To investigate the changes of transient receptor potential polycystic protein 2(TRPP2)in tracheal smooth muscle cells of asthmatic rats and its pathological role in tracheal contraction.Methods The rats were randomly divided into the control group and the asthmatic model group.The animal model of asthma was made by intraperitoneal injection of the newly prepared sensitizing solution.They were intraperitoneally injected on day 1 and day 8,and were sensitized aerosol inhalation of 1%OVA on days 15~20.In the control group,the sensitizing solution was replaced with phosphate buffer solution.Tracheal tension test was conducted to observe the changes of tracheal smooth muscle contraction induced by store-operated calcium entry(SOCE).TRPP2 siRNA was transfected to knock down TRPP2.TRPP2 protein expression was observed by Western Blot and immunohistochemistry.Results After successfully reconstructing the asthma model,the asthma group had significantly higher proportion of SOCE-induced tracheal contraction in hyper potassium-induced contraction than the control group(P<0.05).The expression of TRPP2 protein increased in tracheal smooth muscle cells of asthmatic rats(P<0.05).When TRPP2 siRNA was used to knock down the content of TRPP2,SOCE-induced trachea contraction significantly reduced in the percentage of high-potassium solution-induced trachea contraction in comparison with that of the control group(P<0.05).Conclusion The up-regulated expression of TRPP2 in the tracheal smooth muscle of asthmatic rats may be the main reason for the increased contraction caused by SOCE.
关 键 词:哮喘 气管平滑肌 气管张力 钙库操纵的钙内流 瞬时受体电位多囊蛋白2
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