HORMONAL-REGULATION OF NUCLEAR TYPE-II ESTROGEN-BINDING SITES IN THE DORSOLATERAL PROSTATE OF NOBLE RATS
HORMONAL-REGULATION OF NUCLEAR TYPE-II ESTROGEN-BINDING SITES IN THE DORSOLATERAL PROSTATE OF NOBLE RATS
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DOI：
10.1016/0960-0760(94)00170-q
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发表时间：
1995-03-01
影响因子：
4.1
通讯作者：
YU, M
中科院分区：
文献类型：
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作者：
HO, SM;YU, M
我们先前证明，用雌二醇(E(2))和睾酮(T)同时处理Noble(NBL)大鼠16周后，所有处理动物的前列腺背外侧区(DLP)都能选择性地诱导增殖反应[1，2]。大鼠DLP对雄激素-雌激素联合诱导的有丝分裂作用的独特敏感性可能归因于在这个前列腺叶[2，3]中存在一个中等亲和力、高容量的核雌激素结合蛋白(II型位点)。关于前列腺II型部位的水平是否受激素调节，我们知之甚少。本研究的目的是为了确定睾丸类固醇是否在调节大鼠DLP中基础和/或诱导的II型位点表达水平方面起作用。在第一个实验中，去势大鼠立即用5α-二氢睾酮(DHT)和/或E(2)治疗6周，以确定这些类固醇单独或联合是否能维持去势大鼠DLP中II型位点的水平。DHT和DHT+E(2)对去势大鼠的治疗被发现有效地将DLP II型部位水平和腺体湿重维持在接近完整对照的值，而E(2)治疗未能将这些参数维持在完整动物的水平。在第二个实验中，完整的大鼠被单独或联合使用雄激素(T或DHT)或E(2)治疗16周，以确定哪种激素方案可以在DLP中诱导更高水平的II型位点表达。单独使用雄激素(T或DHT)或E(2)治疗不会改变DLP II型位点的水平，尽管T处理会导致腺体重量轻微增加，而E(2)处理会导致前列腺萎缩。与单一激素处理相反，T+E(2)和DHT+E(2)联合处理在诱导DLP的II型位点加倍和湿重增加方面是有效的。这些数据表明，睾丸雄激素是维持大鼠DLP中II型位点表达基础水平的主要因素，而在组织中诱导更高水平的II型位点表达需要雄激素和雌激素的联合作用。
We previously demonstrated that simultaneous treatment of Noble (NBL) rats with estradiol (E(2)) and testosterone (T) for 16 weeks induces a proliferative response selectively in the dorsolateral prostates (DLP) of all treated animals [1, 2]. The unique sensitivity of rat DLP to the conjoint androgen-estrogen-induced mitogenic action may be attributable to the presence of a moderate affinity, high capacity, nuclear estrogen binder (type II sites) found exclusively in this prostatic lobe [2, 3]. Little is known about whether prostatic type II site levels are under hormonal regulation. The aim of this study is to determine whether testicular steroids play a role in regulating the basal and/or induced levels of type II site expression in rat DLP, In the first experiment, rats were castrated and immediately treated with 5 alpha-dihydrotestosterone (DHT) and/or E(2) for 6 weeks to determine whether these steroids, separately or jointly, could sustain DLP type II site levels in castrates. Treatments of castrated rats with DHT and DHT + E(2) were found to be effective in maintaining DLP type II site levels and gland wet weights at values close to those found in intact untreated controls, while treatments with E(2) failed to maintain these parameters at levels observed in intact animals. In the second experiment, intact rats were treated with an androgen (T or DHT) or E(2), alone or in combination, for 16 weeks to ascertain which hormonal regimen could induce a higher level of type II site expression in the DLP. Treatments of rats with an androgen (T or DHT) or E(2) alone did not change DLP type II site levels even though T treatment caused a slight increase in gland weight, while E(2) treatment induced prostatic atrophy. Contrary to single hormone treatments, combined T + E(2) and DHT + E(2) treatments were effective in inducing a doubling of type II sites and increases in wet weight of the DLPs. These data indicate that testicular androgen is the primary factor responsible for maintaining a basal level of type II site expression in rat DLP, while conjoint androgenic-estrogenic action is needed for the induction of a higher level of type II site expression in the tissue.