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研究生:蔡宜芬
研究生(外文):Yi-Fen Tsai
論文名稱:評估熱水浴對氯化鐵造成大鼠動脈損傷之效應
論文名稱(外文):Evaluation of Hot Spring Effects on FeCl3-Induced Arterial Injury in Rats
指導教授:郭家驊郭家驊引用關係鄭劍廷
學位類別:碩士
校院名稱:臺北巿立體育學院
系所名稱:運動科學研究所
學門:民生學門
學類:運動科技學類
論文種類:學術論文
論文出版年:2007
畢業學年度:95
語文別:中文
論文頁數:73
中文關鍵詞:熱水浴氯化鐵熱休克蛋白氧化壓力抗細胞凋亡蛋白
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規律運動有助於增加心肌中的抗氧化能力、預防或改善疾病及保護心血管;在心血管系統遭遇危急時,如缺血、低氧、氧化壓力及內毒素等,會引發防禦系統的建立以維持細胞恆定,會造成暫時性的蛋白質增加,卻可增加心肌耐受度;本研究為無法規律運動者尋求其他可達到與運動相似效果之輔助方法,來達到保健之效果。利用42℃的熱水浴與時間的應用,探討42℃熱水浴的浸泡方式和血行動力的影響及浸泡次數、浸泡後對氯化鐵造成大鼠動脈損傷之保護效應評估。研究中使用Wistar品系之成年雌性大白鼠;實驗分為兩大部份,第一部分以浸泡面積為區分,分別利用不同面積的熱水浴浸泡,進行血行動力的偵測;第二部分以增加浸泡熱水浴後的時間及浸泡次數來區分,觀察血栓產生時間(Time to occlusion)之長短。結果發現,各組股、頸動脈之TTO依序為control(399±56秒、1313±107秒)、1-24 hr(868±94秒、1836±99秒)、1-72 hr(727±57秒、2109±200秒)、3-24 hr(1015±203秒、2701±453秒)、3-72 hr(1086±208秒、2693±382秒),數值以平均值±標準誤差表示;無論股、頸動脈各實驗組與control達顯著差異(p<0.05);此外減緩血管中氧化壓力(Reactive oxygen species)、黏附因子(Interacellular adhesion molecule-1)、脂質過氧化(4-hydroxy-2-nonenal)及蛋白質過氧化反應(3-nitrotyrosine);增加心血管、肝臟及腎臟各組織中之熱休克蛋白(Hsp70、Hsp60)、抗細胞凋亡蛋白(Bcl-2、Bcl-XL)、抗氧化酵素(MnSOD)。結論,在逐步增加水位的42℃熱水浴刺激下,有助於延緩血栓產生之時間及增加組織中蛋白質表現量,可避免因氧化壓力而導致之心血管疾病。
Regular exercise increases organ/tissue antioxidant activity to prevent and/or ameliorate cardiovascular diseases, and to protect cardiovascular system integrity. Although endogenous defense mechanisms are temporarily and frequently enhanced to increase organ tolerance in response to intense exercise, ischemia, hypoxia, oxidative stress and endotoxin, an appropriate and alternative method for some patients without exercise performance to increase protective potential is necessary. In this study, we developed a progressive 42°C thermal stimulation during 15 min and evaluated the effects of progressive thermal stimulation on systemic hemodynamics and cardiovascular protection after FeCl3-induced arterial injury. In the first part of study, we divided Female Wistar rats into three groups to identify the hemodynamic effects of 42°C whole body thermal stimulation, progressive 42°C thermal stimulation and control rats in this study. We found that in spite of similar anus temperature, the progressive 42°C thermal stimulation ameliorated whole body thermal stimulation-enhanced hypertension and tachycardia. In the second part of study, we used one time or three times of progressive 42°C thermal stimulation in one day to evaluate its protective potential against FeCl3-induced femoral and carotid arterial injury (evaluated by time to occlusion, TTO) after 24 or 72 hours. Our results showed that FeCl3 induced femoral and carotid arterial injury in the endothelial area by producing reactive oxygen species, 3-nitrotyrosine and 4-hydroxynoneal accumulation, and intercellular adhesion molecule I consequently leading to arterial occlusion. TTO level(mean±SE)of femoral and carotid arterial in control(399±56 sec, 1313±107 sec), 1-24 hr(868±94 sec, 1836±99 sec), 1-72 hr(727±57 sec, 2109±200 sec), 3-24 hr(1015±203 sec, 2701±453 sec), 3-72 hr(1086±208 sec, 2693±382 sec). One time or 3 times of progressive 42°C thermal stimulation/day significantly elongated TTO level (P<0.05) and decreased endothelial reactive oxygen species production, 3-nitrotyrosine and 4-hydroxynoneal accumulation, and intercellular adhesion molecule I expression. In addition, 3 times of progressive 42°C thermal stimulation exerted a more efficient protection than one time of progressive 42°C thermal stimulation by the upregulation of heat shock proteins (Hsp60 and Hsp70), antiapoptotic proteins (Bcl-2 and Bcl-xL), and antioxidant Magnesium superoxide dismutase in the cardiovascular tissues, liver and kidney. This study suggests that a modified progressive 42°C thermal stimulation provides an efficiently protective potential against oxidative stress induced cardiovascular diseases.
論文口試委員審定書………………………………………………ii
博碩士論文電子檔案上網授權書………………………………………iii
摘要(中文)………………………………………………………………iv
摘要(英文)………………………………………………………………vi
致謝……………………………………………………………………viii
目錄……………………………………………………………………ix
表目錄……………………………………………………………………xi
圖目錄……………………………………………………………………xii
第一章 緒論……………………………………………………………1
第一節 血管簡介…………………………………………………………3
第二節 調控血管擴張收縮與血管栓塞機制……………………………4
第三節 運動與血管………………………………………………………8
第四節 運動、氧化壓力及疾病……………………………………………9
第五節 熱敷、熱水浴……………………………………………………12
第六節 熱休克蛋白………………………………………………………12
第七節 研究動機…………………………………………………………16
第八節 研究目的…………………………………………………………16
第二章 研究方法與步驟…………………………………………………17
第一節 實驗動物…………………………………………………………17
第二節 實驗分組…………………………………………………………17
第三節 動物氯化鐵傷害模式、流程及計算方式………………………20
第四節 動物手術處理……………………………………………………23
第五節 儀器設備…………………………………………………………23
第六節 實驗藥品及來源…………………………………………………24
第七節 組織切片染色……………………………………………………24
第八節 西方墨點法………………………………………………………28
第九節 統計………………………………………………………………30
第三章 結果………………………………………………………………31
第一節 不同浸泡方式與血行動力變化…………………………………31
第二節 利用氯化鐵誘發血管栓塞及觀察血管血流變化………………31
第三節 有無浸泡熱水浴其血管於不同時間點之變化…………………32
第四章 結論與討論………………………………………………………61
參考文獻…………………………………………………………………65
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