Genazzani A R, Petraglia F, Mercuri N, Brilli G, Genazzani A D, Bergamaschi M, DeRamundo B M, Volpe A
Istituto Clinica Ostetrica e Ginecologica, Università di Modena, Italy.
J Endocrinol Invest. 1990 Feb;13(2):91-6. doi: 10.1007/BF03349515.
The aim of the present study was to evaluate the effects of estrogens and androgens on hypothalamic beta-endorphin (beta-EP) concentrations. Intact or castrated female rats were chronically (2 weeks) treated with estrogen (estradiol benzoate) and/or antiestrogens (clomiphene, cyclophenil or epimestrol), and with androgens (dihydrotestosterone or dehydroepiandrosterone sulphate) and/or antiandrogen (cyproterone acetate). A group of rats treated with vehicle were studied as comparison. The beta-EP concentrations were measured by radioimmunoassay on acidic extracts of rat hypothalami. The administration of clomiphene and cyclophenil significantly reduced hypothalamic beta-EP concentrations in intact rats, while both drugs or estradiol benzoate increased the peptide concentration in castrated rats. Both intact and castrated rats treated with epimestrol showed hypothalamic beta-EP concentrations higher than vehicle treated rats. The estradiol-induced increase of beta-EP was not changed by the concomitant administration of antiestrogens. The administration of dihydrotestosterone significantly decreased beta-EP concentrations in both intact and castrated female rats, while the treatment with dehydroepiandrosterone sulphate only slightly decreased beta-EP levels in intact female rats. The cyproterone acetate-chronically treated rats showed higher beta-EP concentrations than vehicle-treated rats and these changes were reversed by the concomitant addition of dihydrotestosterone or dehydroepiandrosterone sulphate. These results showed that estrogens play a positive role while androgens negatively influence the hypothalamic beta-EP concentrations in female rats, supporting the view that central beta-EP might be a target of gonadal steroid feedback signals.
本研究的目的是评估雌激素和雄激素对下丘脑β-内啡肽（β-EP）浓度的影响。对完整或去势的雌性大鼠长期（2周）给予雌激素（苯甲酸雌二醇）和/或抗雌激素（克罗米芬、环苯丙胺或依普美罗），以及雄激素（双氢睾酮或硫酸脱氢表雄酮）和/或抗雄激素（醋酸环丙孕酮）。以一组给予赋形剂的大鼠作为对照进行研究。通过放射免疫分析法测定大鼠下丘脑酸性提取物中的β-EP浓度。给予克罗米芬和环苯丙胺可显著降低完整大鼠下丘脑β-EP浓度，而这两种药物或苯甲酸雌二醇均可增加去势大鼠的肽浓度。给予依普美罗的完整和去势大鼠下丘脑β-EP浓度均高于给予赋形剂的大鼠。同时给予抗雌激素不会改变雌二醇诱导的β-EP增加。给予双氢睾酮可显著降低完整和去势雌性大鼠的β-EP浓度，而给予硫酸脱氢表雄酮仅略微降低完整雌性大鼠的β-EP水平。长期给予醋酸环丙孕酮的大鼠β-EP浓度高于给予赋形剂的大鼠，同时添加双氢睾酮或硫酸脱氢表雄酮可逆转这些变化。这些结果表明，雌激素起积极作用，而雄激素对雌性大鼠下丘脑β-EP浓度有负面影响，支持中枢β-EP可能是性腺类固醇反馈信号靶点的观点。
