Hirst J J, Rice G E, Jenkin G, Thorburn G D
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Endocrinology. 1988 Mar;122(3):774-81. doi: 10.1210/endo-122-3-774.
The involvement of arachidonic acid and arachidonic acid metabolites in the control of oxytocin secretion by ovine corpus luteum was investigated, using slices of luteal tissue incubated in vitro. Oxytocin was secreted at steady rates by luteal slices, during 60-min incubations (315.0 +/- 45.3 pg/mg.h). The secretion of oxytocin was stimulated by arachidonic acid, phospholipase A2 (PLA2), and phospholipase C (PLC) in a dose-dependent manner. The highest doses of arachidonic acid, PLA2, and PLC used stimulated oxytocin secretion by 145.8 +/- 23.0% (P less than 0.01; n = 6), 331.5 +/- 42.4% (P less than 0.02; n = 4), and 955.5 +/- 278.6% (P less than 0.01; n = 4), respectively. Oxytocin secretion by luteal slices was not affected by either prostaglandin F2 alpha (PGF2 alpha) or PGE2 over a concentration range from 3-3000 nM. Furthermore, inhibitors of the cyclo-oxygenase pathway of arachidonic acid metabolism did not consistently affect arachidonic acid and PLA2-stimulated oxytocin secretion. Nordihydroguaiaretic acid, which inhibits 5-lipoxygenase, however, totally abolished arachidonic acid- and reduced PLA2-stimulated oxytocin secretion. The presence of CoCl2 in the incubation medium also significantly reduced basal and PLA2- and PLC-stimulated oxytocin secretion [P less than 0.05 (n = 5), P less than 0.05 (n = 5), and P less than 0.01 (n = 6), respectively]. We have shown that oxytocin secretion from slices of ovine corpus luteum incubated in vitro is stimulated by exogenous and endogenously released arachidonic acid. The data show that PGF2 alpha and PGE2 do not have a role in luteal oxytocin secretion in vitro and PG formation does not appear to be involved in the stimulation of oxytocin secretion elicited by arachidonic acid or PLA2. Arachidonic acid may have its effect via the lipoxygenase pathway.
利用体外培养的黄体组织切片，研究了花生四烯酸及其代谢产物在调控绵羊黄体催产素分泌中的作用。在60分钟的孵育过程中，黄体切片以稳定的速率分泌催产素（315.0±45.3 pg/mg·h）。花生四烯酸、磷脂酶A2（PLA2）和磷脂酶C（PLC）均以剂量依赖的方式刺激催产素的分泌。所用花生四烯酸、PLA2和PLC的最高剂量分别刺激催产素分泌145.8±23.0%（P＜0.01；n = 6）、331.5±42.4%（P＜0.02；n = 4）和955.5±278.6%（P＜0.01；n = 4）。在3 - 3000 nM的浓度范围内，前列腺素F2α（PGF2α）或前列腺素E2（PGE2）均不影响黄体切片催产素的分泌。此外，花生四烯酸代谢的环氧化酶途径抑制剂并不能始终影响花生四烯酸和PLA2刺激的催产素分泌。然而，抑制5 - 脂氧合酶的去甲二氢愈创木酸完全消除了花生四烯酸和降低浓度的PLA2刺激的催产素分泌。孵育培养基中CoCl2的存在也显著降低了基础以及PLA2和PLC刺激的催产素分泌[分别为P＜0.05（n = 5）、P＜0.05（n = 5）和P＜0.01（n = 6）]。我们已经表明，体外培养的绵羊黄体切片分泌的催产素受到外源性和内源性释放的花生四烯酸的刺激。数据表明，PGF2α和PGE2在体外黄体催产素分泌中不起作用，并且PG的形成似乎不参与花生四烯酸或PLA2引发的催产素分泌刺激。花生四烯酸可能通过脂氧合酶途径发挥作用。
