運動訓練在Zucker肥胖鼠血管保護效果中所扮演的角色; The role of exercise training for vascular protection in obese Zucker rat.

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Title:	運動訓練在Zucker肥胖鼠血管保護效果中所扮演的角色;The role of exercise training for vascular protection in obese Zucker rat.
Authors:	陳立仁;Li-Jen Chen
Contributors:	中國醫藥大學：醫學研究所碩士班
Keywords:	運動訓練;exercise training
Date:	2006-06-21
Issue Date:	2009-08-13 14:50:22 (UTC+8)
Abstract:	活性氧自由基（ROS）已知會造成內皮細胞凋亡及平滑肌細胞增生，研究指出高血脂會抑制粒線體電子傳遞鏈導致細胞內ROS增加。在內皮細胞，ROS會活化Caspase 3相關的凋亡路徑導致凋亡。在平滑肌，ROS會活化ERK 1/2相關增生路徑促進增生。近年來的研究顯示，運動訓練可以藉由提高抗氧化能力來達到對氧化壓力得適應。我們用4～6個月大的雄性Zucker鼠，分成肥胖與瘦兩大組，在個別分出運動與不運動兩組，共四組。將運動組施以每週7天共8週的運動訓練後犧牲。在血管的Western blot實驗中顯示，經過運動訓練後，在肥胖組平滑肌增生以及內皮細胞凋亡的情形有明顯的減少，經過運動訓練之後，抗氧化酵素的表現也有明顯的增加。免疫染色的實驗更加證實，其發生不為以及相同的表現趨勢。在mRNA的表現方面，有著相當有趣的現象，我們發現，ERK的表現與蛋白質的表現是一致的，但是在抗氧化酵素中，發現Cu/Zn SOD在肥胖和運動訓練組中表現量有增加的趨勢，相較於蛋白質的表現只有運動組提高的結果並不一致，我們推測，在高血脂的情形下可能再轉譯的階層有某種程度的影響，另外，Gpx與Catalase的表現在運動組正好相反，因為他們的功能是一樣的所以有取代的效果，至於Mn SOD再各組並無差異，更加證實我們的運動訓練並不造成氧化傷害。總括來說，肥胖組中運動訓練會藉由提高抗氧化能力來減少高血脂所導致之ROS的增加，減少內皮細胞凋亡以及平滑肌細胞增生，並達到血管保護的效果。 Reactive oxygen species (ROS) are known to induced endothelial cell (EC) apoptosis and vascular smooth muscle cell (VSMC) proliferation. It has demonstrated that hyperlipidemia may impact vascular function through increased oxidative stress and synthesized ROS endogenously by inhibiting electron transport chain of mitochodria in vascular cell. In endothelial cells, ROS may activate caspase 3 through mitochondrial pathway then lead EC apoptosis. On the other hand, ROS could produce mitogenic response through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in VSMC. Recent study has observed that exercise training may initiate adaptations to reduce oxidative sources or up regulate antioxidative enzymes. We subjected 4~6 month-old male Zucker rats to an 8-weeks chronic exercise training program on a motorized treadmill. A total of 12 obese rats were randomly divided into two groups, i.e sedentary group and exercise-trained group. All rats were sacrificed at 48 h after the end of their last training session to minimize acute exercise effects from the last training bout. Immunoblot analysis of harvested vessels showed that lower expression of caspase 3 and ERK1/2 in obese exercised group compared with obese standard group. However superoxide dismutase (SOD) and catalase were significantly expression in both obese and lean exercised group. The results of immunohistochemestry shown that caspase 3 and ERK1/2 were highly expression on EC and VSMC both obese sedentary group. Similarly, this phenomenon would be reversed after exercise training. It was very interesting that Cu/ZnSOD and MnSOD mRNA level has no significant change from each group. The mRNA level of glutathione peroxidase was significantly elevated but catalase mRNA level was lowered instead. In conclusion, exercise training plays a role of vascular protection by up regulating antioxidative protein expression and decreasing caspase3 and ERK1/2 protein production in obese Zucker rat.
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