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烟草烟雾诱导大鼠气道黏液糖蛋白分泌过多。

Hypersecretion of mucus glycoproteins in rat airways induced by tobacco smoke.

作者信息

Coles S J, Levine L R, Reid L

出版信息

Am J Pathol. 1979 Mar;94(3):459-72.

Abstract

An animal model of chronic bronchitis has been produced in vivo by exposing rats for 6 weeks to tobacco smoke: the laryngeal and tracheal glands have been studied in vitro by organ culture to analyze glycoprotein precursor incorporation and glycoprotein secretion by individual cells, a feature not previously studied. In the hypertrophied glands produced by tobacco smoke exposure, the cellular rate of glycoprotein secretion was increased. The in vivo administration of phenylmethyloxadiazole (PMO) to rats exposed to tobacco smoke blocked this effect. In vitro analysis of glands from unexposed rats that received PMO showed that it modified cell function directly by reducing the rates both of glycoprotein discharge and or precursor incorporation into intracellular glycoproteins.

摘要

通过让大鼠暴露于香烟烟雾中6周,已在体内建立了慢性支气管炎动物模型:通过器官培养在体外研究了喉和气管腺,以分析单个细胞中糖蛋白前体的掺入和糖蛋白分泌情况,这一特征以前未曾研究过。在因暴露于香烟烟雾而产生的肥大腺体中,糖蛋白的细胞分泌率增加。对暴露于香烟烟雾的大鼠进行体内苯甲基恶二唑(PMO)给药可阻断这种作用。对接受PMO的未暴露大鼠的腺体进行体外分析表明,它通过降低糖蛋白释放率和前体掺入细胞内糖蛋白的速率直接改变细胞功能。

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