THE LIPOXYGENASE INHIBITOR NAFAZATROM INHIBITS STIMULATED PROLACTIN SECRETION IN CULTURED RAT LACTOTROPHS (GH4C1 CELLS)

被引：4

作者：

BJORO, T

LARSEN, V

ENGLUND, K

TORJESEN, PA

HAUG, E

机构：

[1] Hormone Laboratory, Aker Hospital, University of Oslo, Oslo

来源：

SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION | 1992年 / 52卷 / 04期

关键词：

ARACHIDONIC ACID METABOLITES; CAMP; EICOSANOIDES; PITUITARY CELLS; VIP; TRH;

D O I：

10.3109/00365519209088362

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Arachidonic acid metabolites are involved in the regulation of prolactin (PRL) secretion from rat lactotrophs (GH4C1 cells). Phospholipase A2 (PLA2) stimulated PRL secretion, while the PLA2 inhibitor quinacrine reduced both thyrotropin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulated PRL release. Hormonally stimulated PRL release was further increased in the presence of the cyclo-oxygenase inhibitor indomethacin. Nafazatrom, a lipoxygenase inhibitor, reduced stimulated PRL secretion regardless of the mechanism of stimulation [hormonally (VIP and TRH) or by increasing intracellular Ca2+ concentration by KCl or Bay-K and cAMP by forskolin]. None of the inhibitors used in this study had any effect either on the basal PRL secretion or on the production of cAMP. Lipoxygenase products seem to be involved in the regulation of PRL secretion, probably by affecting a late step in the signal transduction.

引用

页码：297 / 303

页数：7

共 34 条

[1] BINDING AND DEGRADATION OF VASOACTIVE-INTESTINAL-PEPTIDE IN PROLACTIN-PRODUCING CULTURED RAT PITUITARY-TUMOR CELLS (GH4C1) [J].