Isohama Y, Kumanda Y, Tanaka K, Kai H, Takahama K, Miyata T
Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.
Jpn J Pharmacol. 1997 Feb;73(2):163-9. doi: 10.1254/jjp.73.163.
Insufficient production of pulmonary surfactant in alveolar type II cells is relevant to many lung diseases. To cure its deficiency, glucocorticoid is commonly used in clinical areas. In the present study, we investigated the effect of dexamethasone on the secretion of phosphatidylcholine, a major phospholipid of pulmonary surfactant, in a primary culture of rat alveolar type II cells. Dexamethasone had no effect on the basal secretion rate of phosphatidylcholine. Dexamethasone augmented both the phosphatidylcholine secretion and the cyclic AMP formation increased by terbutaline. Furthermore, dexamethasone increased the number of beta-adrenoceptors and mRNA expression of beta 2-adrenoceptors in type II cells. These findings indicate that dexamethasone increases pulmonary surfactant secretion through an enhancement of beta 2-adrenoceptor gene expression.
肺泡II型细胞中肺表面活性物质产生不足与多种肺部疾病相关。为治疗其缺乏症，糖皮质激素在临床领域常用。在本研究中，我们在大鼠肺泡II型细胞原代培养物中研究了地塞米松对肺表面活性物质的主要磷脂磷脂酰胆碱分泌的影响。地塞米松对磷脂酰胆碱的基础分泌率没有影响。地塞米松增强了特布他林增加的磷脂酰胆碱分泌和环磷酸腺苷形成。此外，地塞米松增加了II型细胞中β-肾上腺素能受体的数量和β2-肾上腺素能受体的mRNA表达。这些发现表明地塞米松通过增强β2-肾上腺素能受体基因表达来增加肺表面活性物质的分泌。
