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研究生:劉詩蓉
研究生(外文):Liu, Shy-Rong
論文名稱:三碘甲狀腺素與卵巢類固醇激素對調節甲促素及甲釋素分泌之交互作用
論文名稱(外文):Interaction between triiodothyronine and ovarian steroids on the regulation of the release of thyrotropin and thyrotropin-releasing hormone
指導教授:王錫崗王錫崗引用關係
指導教授(外文):Wang, Shyi-Gang
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:生理學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:1994
畢業學年度:82
語文別:中文
中文關鍵詞:生理學三碘甲狀腺素類固醇
外文關鍵詞:PHYSIOLOGY
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本研究的主要目的是利用同時切除卵巢及甲狀腺大鼠來探討活體補償三碘甲狀腺素及卵巢類固醇激素對(1)離體腦下腺前葉釋放甲促素,(2)甲釋素刺激離體腦下腺前葉甲促素分泌,和 (3)高鉀溶液刺激中底下視丘分泌甲釋素的影響,以及 (4)離體處理三碘甲狀腺素與雌二醇對甲釋素刺激腦下腺細胞甲促素分泌的交互作用。鼠同時切除甲狀腺及卵巢後第十天分成八組開始皮下注射三碘甲狀腺素 (每公斤體重注射2微克),雌二醇 (每公斤體重注射25微克),助孕酮(每公斤體重注射10毫克),三碘甲狀腺素與雌二醇,三碘甲狀腺素與助孕酮,雌二醇與助孕酮,或三種激素同時注射。注射生理食鹽水及芝麻油的大鼠當作對照組。連續注射六天,然後斷頸犧牲,收集血樣,取出腦下腺前葉在37℃進行離體培養。腦下腺前葉除經30分鐘基礎培養外,並與甲釋素(30 nM)培養30分鐘,接著與Locke氏培養液培養30分鐘後,再與三碘甲狀腺素(10 nM)或三碘甲狀腺素合併甲釋素(30nM)培養30分鐘。中底下視丘則以60 mM鉀離子培養30分鐘。血漿、培養液及組織萃取液之激素濃度均以放射免疫法檢測甲促素或甲釋素濃度。活體補償三碘甲狀腺素的大鼠,血漿甲促素濃度皆明顯降低,單獨或同時補償雌二醇與助孕酮的大鼠,血漿甲促素濃度與對照組皆無差異。補償三碘甲狀腺素的大鼠離體腦下腺甲促素基礎釋放或經甲釋素刺激的甲促素分泌以及甲促素在腦下腺的含量皆比對照組高。單獨補償雌二醇或助孕酮,或合併補償三碘甲狀腺素及雌二醇,或三種激素同時補償的大鼠,其離體腦下腺甲促素釋放與對照組皆無差異。合併補償三缺甲狀腺素與助孕酮的大鼠則比單獨補償三碘甲狀腺素的大鼠雜體甲促素分泌輕微降低。而離體腦下腺經興三碘甲狀腺素合併甲釋素培養30分鐘後,可抑制甲促素對甲釋素的反應。在離體腦下腺前葉細胞培養中,三碘甲狀腺素同樣可抑制甲促素對甲釋素的反應;預先加入雌二醇培養,則可阻止三碘甲狀腺素抑制甲促素分泌的效應,並呈劑量一反應的表現。單獨活體補償雌二醇的大鼠鐘底下視丘甲釋素分泌與對照組相比顯著增加,單獨活體補償三碘甲狀腺素或助孕酮的大鼠中底下視丘甲釋素分泌比對照組低,同時補償雌二醇與三碘甲狀腺素則可消減三碘甲狀腺素的抑制效果。三種激素同時補償則比單獨雌二醇補償時甲釋素之分泌顯著性增加。以上實驗結果顯示:(1)三碘甲狀腺素抑制血漿甲促素的濃度至少有二條途徑,其一為三碘甲狀腺素且接抑制中底下視丘甲釋素之分泌,其二為三碘甲狀腺素抑制腦下腺前葉甲促素對甲釋素之反應;(2)三碘甲狀腺素補償去卵巢及甲狀腺大鼠造成離體腦下腺前葉甲促素含量增加及釋放增加,可能與甲促素短徑迴鐀抑制甲釋素分泌有關;(3)"卵巢類固醇激素,特別是雌二醇,可能參與三碘甲狀腺素迴鐀調節甲促素與甲釋素的分泌。
It has been well known that thyroidectomy or hypothyroidism increases but administration of thyroid hormones diminishes the concentration of plasma thyrotropin (TSH) in rats. Recently we found that the greater level of thyrotropin-releasing hormone (TRH) in hypophysial portal plasma is decreased by the replacement of thyroxine (T4) in ovariectomized-thyroidectomized (Ovx-Tx) rats. However, the mechanism of thyroid hormones in regulating TSH release by acting at pituitary level is not clear. Since the concentration of plasma TSH is increased by the administration of estradiol benzoate (EB) in either intact or Ovx rats, an interaction between estradiol and thyroid hormones on the secretion of TSH is highly suggested. In the present study, the purpose is to examine (1) the in vivo and in vitro effect of T3 and/or ovarian steroids on the spontaneous and TRH-stimulated release of TSH from APs in vitro. (2) the in vivo effects of T3 and ovarian steroids on TRH release in vitro. Ovx-Tx rats were injected with triiodothyronine (T3, 2 μg/ml/kg), EB (25 μg/ml/kg), progesterone (P, 10 mg/ml/kg), T3 plus EB, T3 plus P, EB plus P, or T3 plus EB and P for 6 days before decapitation. Rats injected with sesame oil and saline were used as control animals. The blood was collected. The anterior pituitary gland (AP) was bisected, and incubated with Locke's medium at 37℃, challenged with TRH (30 nM) , recovery, and then challenged with T3 (10 nM) only or with T3+TRH, 30 min for each interval. Mediobasal hypothalami (MBHs) were challenged with high potassium (60 mM) for 30 min. In another experiment, the APs were enzymatically dispersed and pretreated with or without EB (0, 0.06, 0.6, or 6 nM) for 72 h, and further with T3 (10 nM) for 24 h, followed by an incubation for 30 min with TRH (0, 1, 10, 100 nM). The concentration of TSH in plasma , medium and pituitary tissue samples was measured by radioimmunoassay. The spontaneous and TRH-induced release of TSH in vitro from rat APs, and pituitary TSH content were increased by T3, or T3 plus P as compared with the animals injected with vehicle, or P alone. EB inhibits the effect of T3 on TSH release in vitro. Application of T3 in vitro prevented the release of TSH in response to TRH. EB dose-dependently relieved the inhibitory effect of T3 on TRH-induced TSH release in vitro. TRH release from MBH was increased by EB and inhibited by T3 or P. EB prevented the inhibitory effect of T3 on TRH release. P plus T3 potentiated the stimulatory effects of EB on TRH release. These results suggest that (1) The reduction of the concentration of plasma TSH by T3 is at least in part due to the inhibitory effects of T3 on TRH release from mediobasal hypothalamus, and TSH release in response to TRH. (2) The increased content and release of TSH from the anterior pituitary gland by T3 via an in vivo effect may be involved in a short feedback loop of TSH on TRH release. (3) Ovarian steroids, especially estradiol, play an inhibitory role in regulating T3 effects on the release of TSH and TRH.



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