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催乳素预处理对大鼠黄体膜中前列腺素F2α相关结构变化的影响。

The effect of prolactin pretreatment on prostaglandin F2 alpha-associated structural changes in membranes from rat corpora lutea.

作者信息

Buhr M M, Gruber M Y, Riley J C, Carlson J C

出版信息

Am J Obstet Gynecol. 1983 Jan 15;145(2):263-8. doi: 10.1016/0002-9378(83)90503-3.

DOI:10.1016/0002-9378(83)90503-3
PMID:6571767
Abstract

The ability of prolactin treatment to antagonize the luteolytic effect of prostaglandin F2 alpha (PGF2 alpha) was examined in the rat. Animals were superovulated, treated with PGF2 alpha and various doses of prolactin. Plasma progesterone concentrations were measured to assess luteal function. Microsomes were prepared from ovarian homogenates and examined by wide-angle x-ray diffraction for evidence of structural changes in the cellular membranes during luteolysis. In addition, the concentrations of various lipids were analyzed for alterations in membrane lipid composition. In preparations from control animals, all of the membrane lipid was in the liquid-crystalline phase at body temperature. However, in samples from PGF2 alpha-treated rats, portions of the bilayer underwent a structural alteration from liquid-crystalline to gel phase. This phase transition was not accompanied by significant changes in the relative concentrations of various lipids. Prolactin treatment was effective in inhibiting this membrane breakdown in a dose-dependent manner. These results suggest that PGF2 alpha and prolactin may control luteal function by affecting membrane structure.

摘要

在大鼠中研究了催乳素治疗拮抗前列腺素F2α(PGF2α)黄体溶解作用的能力。对动物进行超排卵处理,用PGF2α和不同剂量的催乳素进行治疗。测量血浆孕酮浓度以评估黄体功能。从卵巢匀浆中制备微粒体,并通过广角X射线衍射检查黄体溶解过程中细胞膜结构变化的证据。此外,分析各种脂质的浓度以检测膜脂质组成的改变。在对照动物的制剂中,所有膜脂质在体温下均处于液晶相。然而,在PGF2α处理的大鼠的样本中,双层的部分区域经历了从液晶相到凝胶相的结构改变。这种相变并未伴随着各种脂质相对浓度的显著变化。催乳素治疗以剂量依赖的方式有效抑制这种膜破坏。这些结果表明,PGF2α和催乳素可能通过影响膜结构来控制黄体功能。

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1
The effect of prolactin pretreatment on prostaglandin F2 alpha-associated structural changes in membranes from rat corpora lutea.催乳素预处理对大鼠黄体膜中前列腺素F2α相关结构变化的影响。
Am J Obstet Gynecol. 1983 Jan 15;145(2):263-8. doi: 10.1016/0002-9378(83)90503-3.
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