Handwerger S, Barry S, Barrett J, Markoff E, Zeitler P, Cwikel B, Siegel M
Endocrinology. 1981 Dec;109(6):2016-21. doi: 10.1210/endo-109-6-2016.
Human decidual explants exposed for 4 h to 150 microM arachidonic acid synthesized and secreted 30.4% (P less than 0.001) and 36.4% (P less than 0.001) less 35S-PRL, respectively, than control explants. Over a 5-h period, the inhibition of PRL secretion was directly proportional to the arachidonic acid concentration at concentrations between 30 and 300 microM (r = 0.91; P less than 0.001). Phospholipase A2 at concentrations of 0.11 and 11.1 U/ml, also inhibited PRL secretion by 46.2 +/- 2.4% (P less than 0.001) and 63.9 +/- 1.4% (P less than 0.001), respectively. Likewise, the fatty acid precursors of arachidonic acid, i.e. linoleic, gamma-linolenic, and dihomo-gamma-linolenic acids, inhibited PRL secretion, but palmitic, oleic, and 11,14,17-icosatrienoic acids and the detergents deoxycholic acid and Triton X-100 had no effects, even at concentrations as high as 300 microM. In contrast, prostaglandins E1, E2, and F2 alpha (3 X 10(-5)-10(12) M each) had no effects on PRL secretion, and the prostaglandin synthetase (cyclooxygenase) inhibitors indomethacin (5 and 25 micrograms/ml) and flufenamic acid (5 micrograms/ml) had no effects on either basal PRL secretion or the inhibitory action of arachidonic acid. These results suggest that arachidonic acid may be involved in the regulation of the synthesis and secretion of decidual PRL. The effect of arachidonic acid, however, does not appear to be mediated by a cyclooxygenase product of arachidonic metabolism.
人蜕膜外植体暴露于150微摩尔花生四烯酸4小时后，与对照外植体相比，合成并分泌的35S - PRL分别减少了30.4%（P < 0.001）和36.4%（P < 0.001）。在5小时期间，在30至300微摩尔浓度范围内，PRL分泌的抑制与花生四烯酸浓度直接成正比（r = 0.91；P < 0.001）。浓度为0.11和11.1单位/毫升的磷脂酶A2也分别抑制PRL分泌46.2±2.4%（P < 0.001）和63.9±1.4%（P < 0.001）。同样，花生四烯酸的脂肪酸前体，即亚油酸、γ-亚麻酸和二高-γ-亚麻酸，抑制PRL分泌，但棕榈酸、油酸、11,14,17-二十碳三烯酸以及去污剂脱氧胆酸和 Triton X-100即使在高达300微摩尔的浓度下也没有作用。相反前列腺素E1、E2和F2α（各为3×10⁻⁵ - 10¹² 摩尔）对PRL分泌没有影响，前列腺素合成酶（环氧化酶）抑制剂吲哚美辛（5和25微克/毫升）和氟芬那酸（5微克/毫升）对基础PRL分泌或花生四烯酸的抑制作用均无影响。这些结果表明花生四烯酸可能参与蜕膜PRL合成和分泌的调节。然而，花生四烯酸的作用似乎不是由花生四烯酸代谢的环氧化酶产物介导的。
