중강도 운동이 고지방식을 유도한 알츠하이머 치매 마우스의 시냅스 소포체 및 항산화 효소 발현에 미치는 영향
Effect of Moderate Intensity Exercise on Synaptic Vesicle Transporter and Antioxidant Enzyme Expression in High Fat Diet Fed 3xTg Mice
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PURPOSE: The purpose of this study was to analyze the effects of aerobic exercise on the expression of synaptic vesicle transporter and antioxidant enzymes in obesity and to investigate the feasibility of exercise training to reduce AD pathogenesis in the 3xTg-AD mice fed a high fat diet. METHODS: Male 3 month old 3xTg-AD mice were divided into standard chow(SC, n=10), standard chow+exercise (SC-EXE, n=10), high fat diet (HFD, n=10), and high fat diet+exercise (HFD-EXE, n=10) groups. EXE mice were subjected to treadmill running at a moderate intensity with duration of 30 minutes per day and frequency of 5 days per week for 12 weeks. HFD mice were fed a 60% fat HFD during the same period. Mice were sacrificed and immunohistology and western blot analysis were performed. RESULTS: Compared with the SC mice, the HFD mice had significantly higher levels of Aβ (p<.01), p-tau/t-tau (p<.01) and defects of Vglut1 (p<.05), VGAT (p<.05), postsynaptic density 95 (p<.01) and GPX (p<.05) in the hippocampus. On the other hand, we found that treadmill running attenuated HFD-induced exacerbations of Aβ (p<.01), p-tau/t-tau (p<.05) and defects of Vglut1 (p<.01), Synaptophysin (p<.05), SOD1 (p<.05) in the hippocampus. CONCLUSIONS: High fat diet-induced obesity resulted in increased AD neuropathology and decreased synaptic vesicle transporter and antioxidant enzyme in the hippocampus of 3xTg-AD mice. However, aerobic exercise delayed AD-like disease progression, alleviated impaired synaptic function and the decreased expression of antioxidant enzymes in the hippocampus.
Abstract
PURPOSE: The purpose of this study was to analyze the effects of aerobic exercise on the expression of synaptic vesicle transporter and antioxidant enzymes in obesity and to investigate the feasibility of exercise training to reduce AD pathogenesis in the 3xTg-AD mice fed a high fat diet. METHODS: Male 3 month old 3xTg-AD mice were divided into standard chow(SC, n=10), standard chow+exercise (SC-EXE, n=10), high fat diet (HFD, n=10), and high fat diet+exercise (HFD-EXE, n=10) groups. EXE mice were subjected to treadmill running at a moderate intensity with duration of 30 minutes per day and frequency of 5 days per week for 12 weeks. HFD mice were fed a 60% fat HFD during the same period. Mice were sacrificed and immunohistology and western blot analysis were performed. RESULTS: Compared with the SC mice, the HFD mice had significantly higher levels of Aβ (p<.01), p-tau/t-tau (p<.01) and defects of Vglut1 (p<.05), VGAT (p<.05), postsynaptic density 95 (p<.01) and GPX (p<.05) in the hippocampus. On the other hand, we found that treadmill running attenuated HFD-induced exacerbations of Aβ (p<.01), p-tau/t-tau (p<.05) and defects of Vglut1 (p<.01), Synaptophysin (p<.05), SOD1 (p<.05) in the hippocampus. CONCLUSIONS: High fat diet-induced obesity resulted in increased AD neuropathology and decreased synaptic vesicle transporter and antioxidant enzyme in the hippocampus of 3xTg-AD mice. However, aerobic exercise delayed AD-like disease progression, alleviated impaired synaptic function and the decreased expression of antioxidant enzymes in the hippocampus.
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