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研究生:陳彥豪
研究生(外文):Chen Yen Hao
論文名稱:甲狀腺荷爾蒙對大鼠腎上腺分泌皮質固酮之影響
論文名稱(外文):Effect of Thyroid Hormones on Corticosterone Secretion in Rats
指導教授:王錫崗先生
指導教授(外文):P. Shyi-Gang Wang
學位類別:碩士
校院名稱:輔仁大學
系所名稱:生物學研究所
學門:生命科學學門
學類:生物學類
論文種類:學術論文
論文出版年:1995
畢業學年度:83
語文別:中文
論文頁數:64
中文關鍵詞:腎上腺腎上腺皮質促素皮質固酮甲狀腺荷爾蒙雌二醇
外文關鍵詞:Adrenal glandAdrenocorticotropic Hormone (ACTH)
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目前已知甲狀腺素可藉由透過下視丘-腦下腺軸線來調節腎上腺分泌皮質
固酮。本研究主要目地是探討甲狀腺素是否直接作用於腎上腺進行激素分
泌的調節。大鼠每日經由皮下注射生理食鹽水、三碘甲狀腺素(T3,每公
斤體重5微克 )或琉尿嘧啶 (PTU,每公斤體重25微克 )連續六天。次日由
頸靜脈注射腎上腺皮質促素(每公斤體重5微克 ),分別在注射前及注射後
收集血樣。另於早上犧牲動物,取得腎上腺進行培養,培養液加入
ACTH(1-24),pACTH及/或T3、T4培養一小時。培養液和血漿以放射免疫測
定法檢測皮質固酮的濃度,另以放射免疫法檢測組織萃取液cAMP濃度。結
果顯示,活體雄鼠在靜脈注射 ACTH後,5分鐘即呈刺激反應。PTU 則不僅
降低皮質固酮基礎值也降低其對 ACTH的反應,T3處理之雄鼠於 ACTH注射
後120分鐘,血漿皮質濃度比對照組低。雌鼠皮質固酮基礎值較雄鼠高,
對ACTH反應較雄鼠慢,T3及PTU則無顯著影響。在離體方面, ACTH(1-24)
及pACTH均對皮質固酮有劑量反應的刺激效果。T3及T4可直接抑制腎上線
分泌皮質固酮而且減少ACTH的刺激效果。活體注射T3並可刺激腎上腺cAMP
之合成。除此,並發現雌雄鼠不論基礎值或是對ACTH的反應皆不同,為了
探討此問題,雌鼠去卵巢十天後,補嘗雌二醇或助孕酮連續三天,第四天
由頸靜脈注入ACTH(1-24)後採血或是斷頭犧牲後取得腎上腺離體培養,刺
激藥物為ACTH(1-24)、T3或ACTH + T3。結果顯示雌二醇及助孕酮均抑制
皮質固酮基礎值,但同時存在時卻提高釋放量。雌二醇或助孕酮個別處理
對 ACTH反應效果明顯。在離體實驗發現助孕酮可直接抑制腎上腺分泌皮
質固酮,而助孕酮及雌二醇均會影響ACTH和T3對腎上腺的作用。 T3可因
劑量之增加而增加腎上腺cAMP之合成。由以上實驗結果,所得結論是
(1)甲狀腺荷爾蒙可藉增加cAMP之合成抑制腎上腺皮質固酮之分泌,(2)助
孕酮及雌二醇對調節血漿皮質固酮基礎值及腎上腺受ACTH刺激分泌皮質固
酮的反應表現交互作用。

Adult rats were injected s.c. with saline, T3 or PTU for 6 days
before challenging with ACTH via the right jugular catheter.
The blood samples were collected after ACTH injection. In the
in vitro study, the AD were collected and incubated with
ACTH(1-24) or pACTH, and/or T3 in the presence or absence of
IBMX for 60 min. The concentration of corticosterone in plasma
and medium and that of cAMP in tissue extracts were measured by
RIA. ACTH(1-24) significantly increased plasma corticosterone 5
min after injection in male rats. PTU reduced the basal and
ACTH-stimulated corticosterone levels in rat plasma.
Administration of T3 reduced the concentration of plasma
corticosterone at 120 min following ACTH enjection. Plasma
corticosterone concentration was higher in female than in male
rats . ACTH resulted in a dose-dependent release of
corticosterone from rat adrenal glands in vitro. Both T3 and T4
decreased corticosterone production in vitro. Administration of
T3 in vivo resulted in an increase of cAMP production in male
rat adrenal glands. Ovx rats injected s.c. with seame oil,
estradiol benzoate (EB), progesterone (P4) or EB+P4 for 3 days
were decapitated or challenged with ACTH via the right jugular
vein. The blood were collected after ACTH(1-24) injection.
After decapitation, rat adrenal glands were excised, bisected
and then incubated with ACTH, T3 or both. We found that either
E2 or P4 reduced, but E2+P4 increased the basal level of plasma
corticosterone. In the vitro study, P4 had a direct effect on
adrenal gland to inhibit corticosterone release. Despite the
presence of E2 and P4, T3 inhibited adrenal gland to release
corticosterone in Ovx rats. However, incubation of T3 induced a
dose-dependent increase of cAMP production in the adrenal
gland. These results suggest that (1) thyroid hormones inhibit
the spontaneous and ACTH-stimulated release of corticosterone
(2) there is an inter- action between E2 and P4 in regulating
corticosterone release.

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