花生四烯酸在糖皮质激素致腭裂作用中发挥作用的进一步证据。

Further evidence for a role of arachidonic acid in glucocorticoid teratogenic action in the palate.

作者信息

Piddington R, Herold R, Goldman A S

出版信息

Proc Soc Exp Biol Med. 1983 Dec;174(3):336-42. doi: 10.3181/00379727-174-41745.

PMID:6420792

Abstract

Arachidonic acid produces a significant reversal of the production of cleft palate by cortisone in the offspring of sensitive strains of mice in vivo. Arachidonic acid in nanogram per milliliter concentrations also produces a significant reversal of the cortisol inhibition of the programmed cell death of the medial edge epithelium of palatal shelves in vitro. This corrective action of arachidonic acid in vitro is significantly blocked by indomethacin at a nanogram per milliliter concentration which selectively inhibits the conversion of arachidonic acid to prostaglandins and/or thromboxanes at the level of cyclooxygenase. These results support the hypothesis that the inhibition of arachidonic acid release and subsequent prostaglandin and/or thromboxane production by glucocorticoids is involved in the teratogenic action of glucocorticoids and demonstrate that one site of this action is the inhibition of epithelial loss.

摘要

花生四烯酸在体内可使敏感品系小鼠后代中由可的松诱导产生的腭裂发生率显著逆转。每毫升纳克浓度的花生四烯酸在体外也可使皮质醇对腭突内侧边缘上皮细胞程序性细胞死亡的抑制作用显著逆转。花生四烯酸在体外的这种纠正作用在每毫升纳克浓度时被吲哚美辛显著阻断，吲哚美辛在环氧化酶水平选择性抑制花生四烯酸转化为前列腺素和/或血栓素。这些结果支持以下假说：糖皮质激素对花生四烯酸释放以及随后前列腺素和/或血栓素生成的抑制作用与糖皮质激素的致畸作用有关，并表明该作用的一个位点是对上皮细胞丢失的抑制。