血小板活化因子与能刺激豚鼠肺泡巨噬细胞中环磷酸腺苷的药物之间的相互作用。

Interaction between PAF-acether and drugs that stimulate cyclic AMP in guinea-pig alveolar macrophages.

作者信息

Bachelet M, Adolfs M J, Masliah J, Bereziat G, Vargaftig B B, Bonta I L

机构信息

Unité de Pharmacologie Cellulaire, INSERM 285, Paris, France.

出版信息

Eur J Pharmacol. 1988 Apr 27;149(1-2):73-8. doi: 10.1016/0014-2999(88)90044-1.

DOI:10.1016/0014-2999(88)90044-1

PMID:2840303

Abstract

The PAF-acether (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine)-induced arachidonate release from alveolar macrophages was significantly reduced by prostaglandin E2 (PGE2) and by the beta-adrenoceptor agonist salbutamol. In addition, PAF-acether markedly reduced the increase in intracellular cyclic AMP (cAMP) concentrations induced by PGE2 and salbutamol. Our data indicate an inverse relationship between intracellular cAMP levels and free arachidonate availability in alveolar macrophages treated with PAF-acether. A rise in intracellular cAMP therefore represents an important alternative route for controlling the effects of PAF-acether and the resulting inflammatory alterations in the respiratory system.

摘要

血小板活化因子（1-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）诱导的肺泡巨噬细胞花生四烯酸释放，被前列腺素E2（PGE2）和β-肾上腺素能受体激动剂沙丁胺醇显著降低。此外，血小板活化因子显著降低了PGE2和沙丁胺醇诱导的细胞内环磷酸腺苷（cAMP）浓度的升高。我们的数据表明，在用血小板活化因子处理的肺泡巨噬细胞中，细胞内cAMP水平与游离花生四烯酸的可用性之间呈负相关。因此，细胞内cAMP的升高代表了控制血小板活化因子的作用以及呼吸系统中由此产生的炎症改变的重要替代途径。