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新型下丘脑花生四烯酸产物刺激正中隆起释放生长抑素。

Novel hypothalamic arachidonate products stimulate somatostatin release from the median eminence.

作者信息

Capdevila J, Chacos N, Falck J R, Manna S, Negro-Vilar A, Ojeda S R

出版信息

Endocrinology. 1983 Jul;113(1):421-3. doi: 10.1210/endo-113-1-421.

Abstract

Arachidonic acid (AA) stimulates the in vitro release of somatostatin (SRIF) from the hypothalamic median eminence (ME). This effect is inhibited by 5, 8, 11, 14-eicosatetraynoic acid (ETYA) but not by indomethacin (ID). Microsomal fractions from the rat hypothalamus catalyze an NADPH-dependent metabolism of AA to form several oxygenated products of which the major metabolites are 5, 6-epoxyeicosatrienoic acid (5, 6-EET) and its hydration product, 5, 6-dihydroxyeicosatrienoic acid (5, 6-DHET). Both novel arachidonate metabolites, particularly 5, 6-EET, are potent in vitro stimuli for the release of SRIF. To a lesser extent, 5, 6-EET is also capable of evoking luteinizing hormone-releasing hormone (LHRH) release. The results suggest that these "epoxygenase" metabolites of AA may be physiologically involved in the control of SRIF release.

摘要

花生四烯酸(AA)刺激下丘脑正中隆起(ME)体外释放生长抑素(SRIF)。5,8,11,14-二十碳四烯酸(ETYA)可抑制此效应,但吲哚美辛(ID)无此作用。大鼠下丘脑微粒体组分催化AA的NADPH依赖性代谢,形成几种氧化产物,其中主要代谢产物是5,6-环氧二十碳三烯酸(5,6-EET)及其水合产物5,6-二羟基二十碳三烯酸(5,6-DHET)。这两种新的花生四烯酸代谢产物,尤其是5,6-EET,是体外刺激SRIF释放的有效物质。5,6-EET在较小程度上也能够引起促黄体生成素释放激素(LHRH)的释放。结果表明,AA的这些“环氧酶”代谢产物可能在生理上参与SRIF释放的调控。

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