激素调节大鼠间质细胞中11β-羟类固醇脱氢酶活性

Hormonal regulation of activity of 11β hydroxys- teroid dehydrogenase

糖皮质激素（大鼠体内是皮质酮）抑制睾丸间质细胞中睾酮合成。１１β－羟类固醇脱氢酶（１１β－ＨＳＤ）通过控制细胞内糖皮质激素浓度调节睾酮合成，并且其活性又能被大鼠内源性皮质酮诱导，由此保护了间质细胞中睾酮的生物合成，使之免于受到糖皮质激素的过度抑制。本研究旨在观察大鼠间质细胞中受１１β－ＨＳＤ调节的两种激素———皮质酮和睾酮是否对培养的大鼠间质细胞中１１β－ＨＳＤ活性及其ｍＲＮＡ表达具有调节作用。结果表明，皮质酮能增加切除肾上腺大鼠培养的间质细胞中１１β－ＨＳＤ氧化酶活性及其ｍＲＮＡ表达。睾酮则明显抑制培养的大鼠间质细胞中１１β－ＨＳＤ氧化酶活性及其ｍＲＮＡ表达。

Glucocorticoids (corticosterone in rat) directly inhibit testosterone biosynthesis in testicular Leydig cells via a receptormediated process.11βhydroxysteroid dehydrogenase (11βHSD) in Leydig cells regulates steroidogenesis by controlling intracellular glucocorticoid concentration.Endogenous corticosterone in rat induces intracellular 11βHSD activity, thereby protecting against glucocorticoidexceed inhibition of testosterone production.The aim of the present study is to observe whether the 11βHSD activity in cultured Leydig cells is modified by two of hormones (corticosterone and testosterone) controlled by this enzyme.The results indicated that corticosterone stimulated 11βHSD oxidative activity mRNA expression in cultured Leydig cells from adrenolectomy.Testosterone significantly inhibited oxidative activity and its mRNA expression in cultured Leydig cells from shamoperated control.