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17β-雌二醇对甲状旁腺激素刺激培养的新生小鼠颅骨骨吸收及前列腺素产生的抑制作用。

Inhibition by 17 beta-estradiol of PTH stimulated resorption and prostaglandin production in cultured neonatal mouse calvariae.

作者信息

Pilbeam C C, Klein-Nulend J, Raisz L G

机构信息

Department of Medicine, University of Connecticut Health Center, Farmington 06032.

出版信息

Biochem Biophys Res Commun. 1989 Sep 29;163(3):1319-24. doi: 10.1016/0006-291x(89)91122-4.

Abstract

Previous attempts to show a direct effect of physiological concentrations of 17 beta-estradiol (beta E2) on bone in vitro have been unsuccessful. We describe a culture system using neonatal mouse calvariae in which beta E2 in the range 1 pM to 1 nM inhibited parathyroid hormone (PTH) stimulated prostaglandin E2 (PGE2) release by 50 to 70% in the presence and absence of cortisol. In addition, beta E2 reduced medium calcium concentration and release of previously incorporated 45Ca by 10 and 20%, respectively, in PTH stimulated cultures. Indomethacin did not block beta E2 effects on resorption. 17 alpha-Estradiol (alpha E2) reduced PTH stimulated 45Ca release but not PGE2 release. Thus, beta E2 has direct effects on bone consistent with its known effects to decrease bone resorption in vivo.

摘要

以往试图证明生理浓度的17β-雌二醇(βE2)在体外对骨骼有直接作用的尝试均未成功。我们描述了一种使用新生小鼠颅骨的培养系统,在该系统中,1皮摩尔至1纳摩尔范围内的βE2在有或没有皮质醇存在的情况下,可使甲状旁腺激素(PTH)刺激的前列腺素E2(PGE2)释放减少50%至70%。此外,在PTH刺激的培养物中,βE2分别使培养基钙浓度和先前掺入的45Ca释放减少了10%和20%。吲哚美辛并未阻断βE2对骨吸收的作用。17α-雌二醇(αE2)减少了PTH刺激的45Ca释放,但未减少PGE2释放。因此,βE2对骨骼有直接作用,这与其在体内降低骨吸收的已知作用一致。

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