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研究生:洪菁霞
研究生(外文):HUNG, CHING-HSIA
論文名稱:漸進式運動訓練誘發熱休克蛋白72對大鼠熱中風及學習記憶的影響
論文名稱(外文):Effect of heat shock protein 72 induced by progressive exercise training on rat heatstroke and memory performance
指導教授:林茂村林茂村引用關係
指導教授(外文):Mao-Tsun Lin
學位類別:博士
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:2004
畢業學年度:92
語文別:中文
論文頁數:190
中文關鍵詞:運動
外文關鍵詞:exercise
相關次數:
  • 被引用被引用:1
  • 點閱點閱:118
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  • 收藏至我的研究室書目清單書目收藏:0
本實驗探討大鼠經過數週漸進式運動訓練之後,在生理方面是否會對熱中風所致的循環性休克及腦缺血性神經細胞損傷產生保護作用?在認知方面是否會對scopolamine所引起的記憶功能缺失產生預防的作用?若有保護作用,是否與運動訓練所誘發體內各重要器官之保護性的HSP72表現有關呢?
將Wistar雄鼠隨機分為漸進式運動訓練組及對照組,運動訓練組動物在跑步機上以每分鐘二十至三十公尺的速度運動三十至六十分鐘,每星期運動五天,如此持續運動一至三週。熱中風之誘發乃將大鼠持續曝露於高溫43℃下,當平均動脈壓(MAP)與局部腦血流量(CBF)自其高點迅速下降之時,視為熱中風生成。結果顯示,運動一或二週無法有效延長熱中風後的存活時間(survival time)和熱中風發作的潛伏期(latency of heatstroke onset),但運動三週卻能有效延長此兩項耐熱性指標,而運動三週之雄鼠體內各重要器官中HSP72之表現約為運動一及二週組的兩倍。十天後,當運動三週之雄鼠體內HSP72之表現量回復至與對照組相當時,其保護效果亦消失了。另外,經過三週運動訓練能有效降低因熱中風引起之腦缺血性神經細胞損傷、血液乳酸值偏高、血液酸鹼值偏低、心血管功能失常、與循環性休克的生成,且對於熱中風形成之後,血液中細胞介質 (TNF-□)的過度增加有抑制的效果。於是我們推論:經過三週運動訓練之大鼠在熱中風後可維持較佳的MAP及CBF,可能是透過體液恆定及心血管功能的維持,而這種現象可能與各重要器官產生大量HSP72有關。
在認知方面以被動制約躲避系統來偵測,結果顯示,經過三週運動訓練之大鼠沒有顯著的對scopolamine所引起的失憶產生預防的效果。於是再以熱處理來誘發大鼠腦中產生大量的HSP72,發現熱處理後16小時(事先誘發大量HSP72)會對scopolamine所引起的失憶,在記憶鞏固與提取階段產生顯著的預防作用。而在接受器結合實驗中,HSP72處理組與對照組在腦中乙醯膽鹼(Ach)接受器之親和力以及Ach接受器之數量上並沒有顯著差異。所以經過三週運動訓練無法在腦中產生足夠的HSP72來對抗scopolamine所引起的學習記憶功能障礙,而大量誘發腦中產生HSP72確實能對抗scopolamine所引起的學習記憶功能缺失,然而此保護作用並非直接作用在Ach接受器層面。
The current study was attempted to assess whether the progressive exercise preconditioning can protect against the heatstroke-induced circulatory shock, and cerebral ischemia and injury, as well as the scopolamine-induced amnesia in rats.
Male Wistar rats were randomly assigned to either a sedentary control group or to an exercise-training group. Trained animals run on a treadmill 5 days/week, 30-60 min/day with intensity 20-30 m/min for 1, 2 or 3 weeks. Heatstroke was induced by exposing the urethane- anesthetized rats to a high blanket temperature of 43℃. The instant at which mean arterial pressure (MAP) and local cerebral blood flow (CBF) decreased from their peak level was taken as the time of heatstroke onset. Prior exercise training for 3 weeks induced about 2-fold increase in HSP72 expression in multiple organs as compared to those training for 1 or 2 weeks. Accordingly, the survival time and latency values during heatstroke in 3-wk-trained rats were significantly greater than those of 1-wk- or 2-wk-trained group. Ten days after 3 weeks exercise training, HSP72 expression in multiple organs returned to the baseline, and then no longer existed the protective effect. The results indicate that 3 weeks progressive exercise may induce HSP72 preconditioning in most vital organs and confer protection against heatstroke-induced circulatory shock and cerebral ischemia.
On the other hand, 3-week progressive exercise preconditioning, although inducing HSP72 in many vital organs, conferred no protection against the scopolamine-induced amnesia. However, heat shock preconditioning, in addition to producing HSP72 overproduction in many vital organs, did protect against the scopolamine-induced amnesia.
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