摘要
本文旨在评价大鼠体内糖皮质激素（大鼠体内是皮质酮）对间质细胞中睾酮合成和１１－β羟类固醇脱氢酶（１１β－ＨＳＤ）活性的影响。为观察内源性皮质酮对间质细胞中睾酮合成的影响，本文测定了切除肾上腺雄性大鼠（４５天龄）血清皮质酮、睾酮，ＬＨ含量和经ＬＨ刺激的纯化间质细胞中睾酮生成量及纯化间质细胞中１１β－ＨＳＤ活性水平。结果表明，切除肾上腺后大鼠血清睾酮水平高于手术对照组及切除后补充皮质酮大鼠。切除肾上腺后大鼠和切除后补充皮质酮大鼠血清ＬＨ水平均无明显变化，表明在上述二实验组中，由于内源性皮质酮变化而导致的间质细胞中睾酮生成的变化不依赖ＬＨ的存在。切除肾上腺后大鼠其纯化的间质细胞睾酮生成量比对照组增加一倍。但经补充皮质酮后睾酮生成量被抑制到对照组水平以下，表明给切除肾上腺后大鼠补充皮质酮能明显地抑制睾酮生成。切除肾上腺后大鼠间质细胞中１１β－ＨＳＤ活性降低，并且这一降低可经补充皮质酮得到恢复。上述结果表明生理性浓度皮质酮对间质细胞中睾酮合成行使直接的负性控制，同时诱导细胞内１１β－ＨＳＤ活性，由此保护间质细胞中睾酮合成免于受到糖皮质激素的过度抑制。
The aim of the present study was to assess the effect of glucocorticoids (corticosterone, B, in the rat) at physiological levels in rat on Leydig cells steroidogenesis and 11β-hydroxysteroid dehydrogenase (11β-HSD) activities. To observe the effect of endogenous B on the testosterone (T) production. B, T and LH were measured in serum of the male adrenalectomized (ADX) rats. T production was meassured in aliquots of spent culture media from 3-hours incubations of purified Leydig cells with LH-stimulation. The levels of 11β-HSD activity were meassured in purified Leydig cells. ADX rats had decreased serum B and elevated T in contrast to control or ADX rats that B replacement ( P >0.05). Serum LH levels were uninfluenced by ADX rats, with or without B replacement ( P >0.05). This indicated that the alteration of T production in Leydig cells, owing to the change of endogenous B, was induced by a mechanism that is independent of LH. ADX rats nearly doubled LH-stimulated T production by purified Leydig cells. T production by Leydig cells from the ADX rats with B treatment was lower than control values, indicating that B inhibits T production after ADX. The activity of 11β-HSD in Leydig cells declined after ADX. The decline in 11β-HSD activities after ADX was prevented by B replacement. We conclude that physiological levels of B exert a tonic, negative control directly on Leydig cell steroidogenesis and also induce intracellular 11β-HSD activity, thereby protecting against glucocorticoid-exceed inhibition of T production.
基金
洛克菲勒基金
