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糖皮质激素抑制大鼠前体细胞型睾丸间质细胞的类固醇生成。

Glucocorticoid suppresses steroidogenesis in rat progenitor Leydig cells.

作者信息

Xiao Ye-Chen, Huang Ya-Dong, Hardy Dianne O, Li Xiao-Kun, Ge Ren-Shan

机构信息

Population Council, New York, NY 10065, USA.

出版信息

J Androl. 2010 Jul-Aug;31(4):365-71. doi: 10.2164/jandrol.109.009019. Epub 2010 Jan 14.

Abstract

Glucocorticoid (GC) inhibits testosterone production in adult Leydig cells by the glucocorticoid receptor (GR). However, whether GC affects the development of Leydig cells is unclear. The goal of the present study is to investigate the effects of GC on steroidogenesis of rat progenitor Leydig cells (PLCs) in vitro. Dexamethasone (DEX) inhibited androsterone (AO) production in PLCs. The GR antagonist RU38486 reversed the DEX-induced inhibition of AO, whereas the mineralocorticoid receptor antagonist RU28318 did not. RU38486 also reversed DEX-induced reductions in steady-state mRNA levels of steroidogenic acute regulatory protein (Star) and 3β-hydroxysteroid dehydrogenase 1 (Hsd3b1). Steroidogenic acute regulatory protein (StAR) protein expression and 3β-hydroxysteroid dehydrogenase (3βHSD) enzyme activity were affected similarly. These results show that GCs inhibit steroidogenesis of PLCs by suppression of StAR and 3βHSD via a GR-mediated mechanism.

摘要

糖皮质激素(GC)通过糖皮质激素受体(GR)抑制成年睾丸间质细胞中的睾酮生成。然而,GC是否影响睾丸间质细胞的发育尚不清楚。本研究的目的是在体外研究GC对大鼠前体睾丸间质细胞(PLCs)类固醇生成的影响。地塞米松(DEX)抑制了PLCs中的雄酮(AO)生成。GR拮抗剂RU38486逆转了DEX诱导的AO抑制作用,而盐皮质激素受体拮抗剂RU28318则没有。RU38486还逆转了DEX诱导的类固醇生成急性调节蛋白(Star)和3β-羟基类固醇脱氢酶1(Hsd3b1)稳态mRNA水平的降低。类固醇生成急性调节蛋白(StAR)蛋白表达和3β-羟基类固醇脱氢酶(3βHSD)酶活性受到类似影响。这些结果表明,GC通过GR介导的机制抑制StAR和3βHSD,从而抑制PLCs的类固醇生成。

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