论文部分内容阅读
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。
This article aims to evaluate the effects of rat glucocorticoid (corticosterone in rats) on testosterone synthesis and 11-beta hydroxysteroid dehydrogenase (11 beta-HSD) activity in stromal cells. In order to observe the effect of endogenous corticosterone on testosterone synthesis in stromal cells, we measured serum corticosterone, testosterone and LH levels in adrenalectomized male rats (45 days old) and testosterone production in purified stromal cells stimulated by LH And the level of 11β-HSD activity in purified stromal cells. The results showed that the level of serum testosterone in rats after adrenalectomy was higher than that in the control group and corticosterone-supplemented rats. There was no significant change in serum LH levels between the adrenalectomized rats and the corticosterone-supplemented rats, indicating that the changes in testosterone production in interstitial cells independent of endogenous corticosterone in the above two experimental groups are independent of LH The presence. After the removal of the adrenal gland, the amount of purified testosterone in the stromal cells of the rats was double that of the control group. However, testosterone production was suppressed below the level of control by corticosterone supplementation, indicating that corticosterone replacement in rats adrenalectally markedly inhibited testosterone production. 11β-HSD activity is reduced in interstitial cells of rat after excision of the adrenal gland, and this reduction can be restored by corticosteroid supplementation. The above results indicate that physiological concentrations of corticosterone exert a direct negative control on testosterone synthesis in stromal cells while inducing intracellular 11 [beta] -HSD activity thereby protecting testosterone synthesis in interstitial cells from over-inhibition by glucocorticoids.