DIRECT INHIBITORY EFFECT OF GLUCOCORTICOIDS UPON TESTICULAR LUTEINIZING-HORMONE RECEPTOR AND STEROIDOGENESIS INVIVO AND INVITRO
DIRECT INHIBITORY EFFECT OF GLUCOCORTICOIDS UPON TESTICULAR LUTEINIZING-HORMONE RECEPTOR AND STEROIDOGENESIS INVIVO AND INVITRO
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DOI：
10.1210/endo-108-6-2142
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发表时间：
1981-01-01
期刊：
影响因子：
4.8
通讯作者：
HSUEH, AJW
中科院分区：
文献类型：
--
作者：
BAMBINO, TH;HSUEH, AJW
在体内和体外研究了糖皮质激素对睾丸黄体生成素受体含量和类固醇生成的直接影响。用不同剂量的地塞米松、皮质酮或合成孕激素17，21-dimethyl-19-nor-pregna-4，9-diene-3，20-dione(R5020)处理未成熟的垂体切除大鼠。一些动物还同时给予FSH(卵泡刺激素)治疗，以防止垂体切除所致的睾丸功能下降。治疗5天后，采用[125I]hCG结合法测定睾丸组织中促黄体生成素/人绒毛膜促性腺激素受体的含量，并通过体外孵育法测定睾丸的促性腺激素生成反应。地塞米松降低对照组和FSH处理组大鼠的睾丸黄体生成素受体，皮质酮(10微克/天)降低FSH处理组大鼠的睾丸黄体生成素受体，但对未用FSH处理的大鼠无影响。R5020对睾丸促黄体生成素受体含量无影响。在体内，用FSH处理去垂体的大鼠，在体外增加了基础的和hCG刺激的雄烷二醇的产生。同时使用地塞米松治疗，而不是R5020，同时减少基础和hCG刺激的睾丸雄激素的产生。在成年去垂体大鼠睾丸细胞的原代培养中，还研究了糖皮质激素对睾丸类固醇生成潜能的直接影响。用人绒毛膜促性腺激素处理培养的睾丸细胞可增加睾酮的产生。在hCG处理的细胞中加入各种天然和合成的糖皮质激素，而不是R5020，以剂量和时间相关的方式减少睾酮的产生(曲安奈德。地塞米松；皮质醇。皮质酮)。在加入10-7M地塞米松后6h，hCG处理细胞的睾酮产量明显下降40%。糖皮质激素对睾丸黄体生成素受体含量和类固醇合成有直接的抑制作用，提示肾上腺皮质激素可能对睾丸功能有调节作用。
The direct effects of glucocorticoids on testicular LH [luteinizing hormone] receptor content and steroidogenesis were studied in vivo and in vitro. Immature hypophysectomized rats were treated with varying doses of dexamethasone, corticosterone, or a synthetic progestin, 17,21-dimethyl-19-nor-pregna-4,9-diene-3,20-dione (R5020). Some animals were also treated concomitantly with FSH [follicle stimulating hormone] to prevent the hypophysectomy-induced decrease in testis functions. At the end of 5 days of treatment, testicular LH/hCG [human chorionic gonadotropin] receptor content was measured by [125I]hCG binding assay while steriodogenic responsiveness was measured by in vitro incubation of testes. Dexamethasone decreased testicular LH receptor in control and FSH-treated hypophysectomized rats in doses as low as 10 .mu.g/day; corticosterone (10 .mu.g/day) decreased testicular LH receptor in the FSH-treated rats but had no effect in rats not treated with FSH. R5020 had no effect on testicular LH receptor content. In vivo treatment of hypophysectomized rats with FSH increased both basal and hCG-stimulated production of androstanediol in vitro. Concomitant treatment with dexamethasone, but not R5020, decreased both basal and hCG-stimulated testicular androstanediol production. The direct effect of glucocorticoids on testicular steroidogenic potentials was also studied in primary culture of testicular cells obtained from adult hypophysectomized rats. Treatment of cultured testicular cells with hCG increased testosterone production. The addition of various natural and synthetic glucocorticoids, but not R5020, to hCG-treated cells decreased testosterone production in a dose- and time-related manner (triamcinolone .gtoreq. dexamethasone > cortisol .gtoreq. corticosterone). A 40% decrease in testosterone production was apparent at 6 h after addition of 10-7 M dexamethasone to hCG-treated cells. The direct inhibitory effect of glucocorticoids on testicular LH receptor content and steroidogenesis is demonstrated suggesting the adrenal glucocorticoids may regulate testis functions.