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作 者:刘峰[1] 周向东[1] 李琪[1] 刘美花[1] 王杰[1] Liu Feng;Zhou Xiangdong;Li Qi;Liu Meihua;Wang Jie(Department of RespiratoU Medicine,The First Affiliated Hospital of Hainan Medical University,Haikou,Hainan,China 570102)
机构地区:[1]海南医学院第一附属医院呼吸内科,海南海口570102
出 处:《中国药业》2018年第21期5-8,共4页China Pharmaceuticals
基 金:国家自然科学基金[81660010];国家自然科学基金[8161101480];海南省自然科学基金[20168305];海南省卫生厅科研课题[16A200021];海南医学院培育基金[HY2016-16]
摘 要:目的探讨苦味素受体(T2Rs)在PM2. 5(particles with an aerodynamic diameter of less than 2. 5μm)刺激诱导的气道上皮细胞黏液高分泌中的干预机制。方法通过培养人气道上皮细胞,构建气道黏液高分泌模型,以PM2. 5为刺激因素,桔梗皂苷为干预因素,采用细胞免疫荧光法、酶联免疫吸附(ELISA)法及RT-PCR法,分别检测各组人气道上皮细胞中T2R14和气道上皮细胞黏蛋白(MUC) 5AC的蛋白表达情况及m RNA水平。结果 PM2. 5组MUC5AC的蛋白表达情况及m RNA水平较对照组显著升高,T2R14的蛋白表达情况及m RNA水平变化不明显;桔梗皂苷干预组MUC5AC的蛋白表达情况及m RNA水平较PM2. 5组显著下降,T2R14的蛋白表达情况及m RNA水平较对照组升高。结论中药的苦味物质刺激可引起人气道上皮细胞T2R14的激活表达,并通过阻断气道黏蛋白的生成和分泌,从而达到抑制气道黏液高分泌的目的。Objective To investigate the mechanism of bitter taste receptor(T2Rs) on mucin hypersecretion induced by particles with an aerodynamic diameters of less than 2.5 μm(PM2. 5) in air-way epithelial cells. Methods Bronchial epithelial cells were cultured to construct the model of air-way mucus hypersecretion, and then stimulated by PM2. 5, platycodin was taken as intervention factor. The expressions of T2R14 and MUC5AC protein were detected by immunofluorescence method and ELISA method respectively. The levels of T2R14 and MUC5AC mRNA were measured by RT- PCR. Results The expression of MUC5AC protein and level of MUC5AC mRNA in the PM2.5 group were significantly higher than those in the control group, the expression of T2R14 protein and level of T2R14 mRNA were not changed obviously. The expression of MUC5AC protein and level of MUC5AC mRNA in platycodin intervention group were significantly lower than those in PM2.5 group, while the expression of T2R14 protein and level of T2R14 mRNA were significantly higher than those in the control group. Conclusion The components of bitter Chinese medicine may induce activating and expressing of human bronchial epithelial cells T2R14, and then inhibit the air-way hypersecretion via blocking MUC5AC production and secretion.
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