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研究生:何項成
研究生(外文):Xiang-Cheng He
論文名稱:雌激素,三價鉻離子及合併使用兩者對於子宮卵巢摘除后的母鼠血清中血管加壓素的影響
論文名稱(外文):The effects of estrogen, trivalent chromium and combination of estrogen and trivalent chromium on the level of vasopressin in serum of ovariohysterectomized rats
指導教授:李衛民李衛民引用關係
指導教授(外文):Wei-Ming Lee
口試委員:李衛民賴政宏吳瑞得
口試委員(外文):Wei-Ming LeeCheng-Hung LaiJui-Te, Wu
口試日期:2017-06-07
學位類別:碩士
校院名稱:國立中興大學
系所名稱:獸醫學系所
學門:獸醫學門
學類:獸醫學類
論文種類:學術論文
論文出版年:2017
畢業學年度:105
語文別:英文
論文頁數:37
中文關鍵詞:血管加壓素雌激素三價鉻離子大鼠
外文關鍵詞:vasopressinestrogentrivalent chromiumrat
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血管加壓素(VP)是一種神經垂體後葉產生的荷爾蒙,同時它也是一種抗利尿激素。血管加壓素廣泛參與了機體的生理調節過程,包括腎臟的水份重吸收,心血管系統的的動態平衡,腦下垂體前葉的荷爾蒙分泌。血管加壓素經由血管加壓素受體V1a,V1b和V2來調控效應器官和靶細胞。V2受體位於腎臟遠曲小管和集尿管,起到刺激水份重吸收的作用。V1a受體在腎臟中起到維持尿量的作用,與V2受體引起的抗利尿功能相互拮抗。另外,在血管加壓素的基因上存在一個雌激素應答元件,因而雌激素的使用會導致鈉和水份的蓄積,從而可能進一步影響血管加壓素的功能。與此同時,三價鉻離子(Cr3+)在體內碳水化合物,脂肪和蛋白質的代謝過程中扮演了重要的角色。鉻離子能夠強化胰島素的作用,同時胰島素功能加強導致血管緊張程度下降。於是,本實驗的目標在於探究聯合使用雌激素以及鉻離子對於血清中血管加壓素濃度的影響。實驗採用37隻雌性SD大鼠。所用大鼠在摘除其子宮卵巢后,隨機分為六個組別:(1)三價鉻離子組;(2)低劑量(0.025 mg/kg)雌激素組;(3)高劑量(0.5 mg/kg)雌激素組;(4)三價鉻離子合併低劑量雌激素組;(5)三價鉻離子合併高劑量雌激素組;(6)對照組。所用藥物都每天經口服灌飼。在實驗進行到第十二週時,採集大鼠的腎臟組織及血清樣本。根據結果,低劑量雌激素組,高劑量雌激素組及對照組,它們的血清中血管加壓素的濃度之間並無顯著區別。然而,在合併使用雌激素及三價鉻離子的兩組中,鉻離子合併高劑量雌激素組的血清血管加壓素的濃度(93.4±32.5 pg/ml) 顯著低於鉻離子合併低劑量雌激素組(163.0±37.0 pg/ml)。我們同時觀察隨著雌激素劑量的增加,大鼠血清中血管加壓素的的濃度產生下降。之前的研究者也指出長期的雌激素使用會導致液體在體內的蓄積。除了以上的結果,在單獨給予三價鉻離子后,大鼠的血清血管加壓素濃度沒有顯著地改變。根據以上的結果,我們得出長期的雌激素給予,會造成液體蓄積,進而導致了血清中血管加壓素的下降。在大鼠上單獨使用三價鉻離子不會對血清中血管加壓素造成顯著地改變,但是三價鉻離子可能參與了由雌激素造成的液體蓄積的過程。至於它的機制還需要進一步的研究。
The neurohypophysial hormone vasopressin (VP), also known as an antidiuretic hormone, is involved in a wide range of physiological regulatory processes, including renal water reabsorption, cardiovascular homeostasis, hormone secretion from the anterior pituitary. Target organs and cells perceive hormonal stimuli by vasopressin (VP) through three distinct VP receptors, V1a, V1b, and V2. The V2 receptor is located in the renal distal tubules and collecting ducts, and stimulates water absorption. V1a receptor plays a role in maintaining urine flow for renal function by acting against V2 receptor-mediated anti-diuresis. In addition, the VP gene has an estrogen response element, and estrogen administration led to sodium and fluid retention, which may influence the function of VP further. Meanwhile, trivalent chromium (Cr3+) is an important element which involved in the metabolism of lipid, proteins and carbohydrates. It also has positive effects on insulin, which can attenuate vasoconstriction. Hence, the aim of this study is to figure out the effects of combination between estrogen and Cr3+ on the level of serum vasopressin. Thirty-seven female Sprague-Dawley(SD) rats, all of which were ovariohysterectomy and randomly divided into six groups: (1) Cr3+ group; (2) low-dose estrogen (0.025 mg/kg) group; (3) high-dose estrogen (0.5 mg/kg) group; (4) Cr3+ with low-dose estrogen group; (5) Cr3+ with high-dose estrogen group; (6) control group. All drugs were administered by force feeding every day. Serum and kidneys were collected from them at 12th week. In the results, there was no observable difference between low-dose estrogen group, high-dose estrogen group and control group on the concentration of serum vasopressin. However, there was a significant difference on level of serum VP between the Cr3+ with low-dose estrogen group (163.0±37.0 pg/ml) and Cr3+ with high-dose estrogen group (93.4±32.5 pg/ml), and our study indicates a negative correlation between the dose of estrogen and the level of serum VP. Apart from these findings, there was no significant change on serum VP after Cr3+ treatment. According to all results, Long-time administration of estrogen cause fluid retention, which results in decreasing of serum vasopressin. Independent Cr3+ administration on rats will not cause observable change on concentration of serum vasopressin. But Cr3+ might participate in fluid retention caused by estrogen in rats, which’s mechanism need to be studied by further research.
摘要...................................................................i
Abstract.........................................................iii
Content..........................................................v
List of tables................................................vi
List of figures ............................................vii
Chapter 1 Introduction...........................1
Chapter 2 Materials and methods....12
Chapter 3 Results....................................16
Chapter 4 Discussion.............................28
Chapter 5 Conclusions..........................30
Reference...................................................31
Appendix....................................................37
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