BACKGROUND It is an established fact that excess of glucocorticoids could cause the harmful effects, such as suppression on the male reproduction. Although glucocorticoids pharmacologically inhibit the Leydig cell function, their roles in Leydig cell development are unclear. Therefore, the present study was designed to investigate effects of synthetic glucocorticoid dexamethasone (DEX) on rat stem Leydig cell proliferation and differentiation. METHODS Male Sprague-Dawley rats received a single intraperitoneal injection of 75 mg/kg EDS to eliminate Leydig cells and an in vitro culture system of the seminiferous tubules was established from Leydig cell-depleted testis. Using basal medium and Leydig cell differentiation-inducing medium (LIM) in the culture system, we examined the effects of DEX (0-100 nM) on the proliferation and differentiation of the stem Leydig cells in vitro, respectively. RESULTS Results showed that LIM is a good agent to induce stem Leydig cell differentiation into Leydig cells that produce testosterone in vitro. DEX inhibited the differentiation of stem Leydig cells by reducing the expression levels of Cyp17a1 and Scarb1 and that NR3C1 antagonist RU38486 reversed the DEX-mediated effects. However, DEX are not involved with the proliferation of stem Leydig cells. CONCLUSIONS DEX suppressed the differentiation of rat Leydig cells in vitro and glucocorticoid-induced effects acted through NR3C1. This suppression partially targets on Cyp17a1 and Scarb1 gene expression.

中文翻译：

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地塞米松在体外抑制大鼠睾丸间质干细胞的分化。

背景技术已经确定的事实是，过量的糖皮质激素会引起有害作用，例如抑制雄性生殖。尽管糖皮质激素在药理学上抑制Leydig细胞功能，但它们在Leydig细胞发育中的作用尚不清楚。因此，本研究旨在研究合成的糖皮质激素地塞米松（DEX）对大鼠干Leydig细胞增殖和分化的影响。方法雄性Sprague-Dawley大鼠接受腹膜内注射75 mg / kg EDS以消除Leydig细胞，并从Leydig细胞耗尽的睾丸中建立了曲细精管的体外培养系统。在培养系统中使用基础培养基和Leydig细胞分化诱导培养基（LIM），我们分别检查了DEX（0-100 nM）对体外培养的干Leydig细胞增殖和分化的影响。结果结果表明，LIM是诱导干Leydig细胞分化为体外产生睾丸激素的Leydig细胞的良好药物。DEX通过降低Cyp17a1和Scarb1的表达水平来抑制干Leydig细胞的分化，而NR3C1拮抗剂RU38486则逆转了DEX介导的作用。但是，DEX不参与干Leydig细胞的增殖。结论DEX抑制了大鼠Leydig细胞的体外分化，糖皮质激素通过NR3C1发挥了作用。此抑制部分针对Cyp17a1和Scarb1基因表达。结果结果表明，LIM是诱导干Leydig细胞分化为体外产生睾丸激素的Leydig细胞的良好药物。DEX通过降低Cyp17a1和Scarb1的表达水平来抑制干Leydig细胞的分化，而NR3C1拮抗剂RU38486则逆转了DEX介导的作用。但是，DEX不参与干Leydig细胞的增殖。结论DEX抑制了大鼠Leydig细胞的体外分化，糖皮质激素通过NR3C1发挥了作用。此抑制部分针对Cyp17a1和Scarb1基因表达。结果结果表明，LIM是诱导干Leydig细胞分化为体外产生睾丸激素的Leydig细胞的良好药物。DEX通过降低Cyp17a1和Scarb1的表达水平来抑制干Leydig细胞的分化，而NR3C1拮抗剂RU38486则逆转了DEX介导的作用。但是，DEX不参与干Leydig细胞的增殖。结论DEX抑制了大鼠Leydig细胞的体外分化，糖皮质激素通过NR3C1发挥了作用。此抑制部分针对Cyp17a1和Scarb1基因表达。但是，DEX不参与干Leydig细胞的增殖。结论DEX抑制了大鼠Leydig细胞的体外分化，糖皮质激素通过NR3C1发挥了作用。此抑制部分针对Cyp17a1和Scarb1基因表达。但是，DEX不参与干Leydig细胞的增殖。结论DEX抑制了大鼠Leydig细胞的体外分化，糖皮质激素通过NR3C1发挥了作用。此抑制部分针对Cyp17a1和Scarb1基因表达。