Role of arachidonic acid or its metabolites in growth-hormone-releasing factor-induced release of somatostatin from the median eminence.
Role of arachidonic acid or its metabolites in growth-hormone-releasing factor-induced release of somatostatin from the median eminence.
复制标题
花生四烯酸或其代谢物在生长激素释放因子诱导的生长抑素从中隆起释放中的作用。
DOI：
10.1159/000125592
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发表时间：
1990
影响因子：
4.1
通讯作者：
Snyder,GD
中科院分区：
文献类型：
--
作者：
Aguila,MC;Milenkovic,L;McCann,SM;Snyder,GD
使用体外培养系统在成年雄性大鼠中评估花生四烯酸（AA）释放可能参与生长激素释放因子（GRF）诱导的下丘脑正中隆起（ME）释放生长抑素（SRIF）。 ME与[14C]-AA预孵育，然后洗涤并与媒介物或测试试剂一起孵育，并测量SRIF和[14C]-AA向培养基中的释放。在仅为确定 SRIF 释放而设计的实验中，ME 首先预孵育 30 分钟。然后丢弃培养基并用新鲜缓冲液或测试物质替换并孵育10、20和/或30分钟。 GRF (10–10M) 在 20 分钟内显着刺激 AA 和 SRIF 释放，最大释放发生在 30 分钟。 GRF 对 AA 释放的刺激作用与 SRIF 的释放一致。磷脂酶 A2 抑制剂（10-6M，奎纳克林）完全消除了 GRF 对 AA 和 SRIF 释放的刺激作用。 GRF 诱导的 SRIF 释放也受到吲哚美辛（10-6M，一种环氧合酶抑制剂）和美替拉酮（10-6M，一种细胞色素 P-450 抑制剂）的抑制。另一方面，去甲二氢愈创木酸（10-6M，一种脂氧合酶抑制剂）对 GRF 诱发的 SRIF 释放没有影响。这里提供的数据表明，导致 SRIF 分泌的一个重要的 GRF 介导事件是体外 ME 片段中 AA 的释放增加。总之，我们的数据表明，GRF 对 SRIF 释放的刺激作用部分归因于 AA 的释放和随后代谢为一种或多种代谢物。
The possible involvement of arachidonic acid (AA) release in growth-hormone-releasing factor (GRF)-induced somatostatin (SRIF) release from the median eminence (ME) of the hypothalamus was evaluated in adult male rats using an in vitro incubation system. The MEs were preincubated with [14C]-AA, then washed and incubated with vehicle or test agents, and the release of SRIF and [14C]-AA into the medium was measured. In the experiments designed only to determine SRIF release, the MEs were first preincubated for 30 min. The medium was then discarded and replaced with fresh buffer or test substances and incubated for 10, 20 and/or 30 min. GRF (10–10M) stimulated both AA and SRIF release significantly within 20 min, with maximum release occurring at 30 min. The stimulatory effect of GRF on AA release was coincident with the release of SRIF. A phospholipase A2inhibitor (10–6M, quinacrine) completely abolished the stimulatory effect of GRF on both AA and SRIF release. The release of SRIF induced by GRF was also inhibited by both indomethacin (10–6M, a cyclooxygenase inhibitor) and metyrapone (10-6M,a cytochrome P-450 inhibitor). On the other hand, nordihydroguaiaretic acid (10–6M, a lipoxygenase inhibitor) had no effect on GRF-evoked SRIF release. The data presented here suggest that an important GRF-mediated event leading to SRIF secretion is an elevated release of AA from ME fragments in vitro. In conclusion, our data are suggestive that the stimulatory effect of GRF on SRIF release is due, in part, to the release and subsequent metabolism of AA to one or more metabolites.