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首页> 外文期刊>International Journal of Environmental Research and Public Health >Effects of Long-Term Endurance Exercise and Lithium Treatment on Neuroprotective Factors in Hippocampus of Obese Rats
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Effects of Long-Term Endurance Exercise and Lithium Treatment on Neuroprotective Factors in Hippocampus of Obese Rats

机译:长期耐久性运动与锂处理对肥胖大鼠海马神经保护因子的影响

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To investigate the effects of long-term lithium treatment and low intensity endurance exercise on brain-derived neurotrophic factor (BDNF) expression and glycogen synthase kinase 3 beta (GSK3β) activity in the hippocampus of obese rats. Fifty 10-week-old male Sprague-Dawley rats were selected. There was a control group of 10 rats (chow control group) while the other forty rats were fed on a high-fat diet for eight weeks to induce obesity. Rats were then assigned into four random groups. The rats were given 10 mg/kg lithium chloride (LiCl) dissolved in 1 mL sterile distilled water once a day, 5 times a week. The rats did 20 min of treadmill walking with an exercise intensity of 40% maximal oxygen uptake (VO 2 max) (12 m/min, slope 0%). This was performed for 20 min a day, 3 days a week. Twelve weeks of lithium treatment or endurance exercise significantly reduced body weight and body fat mass in obese rats, without showing additive effects when the treatments were given in parallel or significant toxic responses in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in blood and kidney and liver tissues. BDNF expression in the hippocampus was significantly increased both in exercise and lithium groups with synergistic effects found in the group where both exercise and lithium treatments were given in parallel. On the other hand, the decrease in GSK3β activity was shown only in the lithium treatment group, without showing additive effects when the treatments were given in parallel. Lithium and low-intensity endurance exercise for 12 weeks increased the expression of BDNF, a neuroprotective factor in the hippocampus of obese mice. Lithium treatment alone inhibited the activity of GSK3β. This can be interpreted as a positive indication of applicability of the two factors in the prevention of neurodegenerative diseases.
机译:探讨长期锂处理和低强度耐久性运动对肥胖大鼠海马脑衍生的神经营养因子(BDNF)表达和糖原合酶激酶3β(GSK3β)活性的影响。选择了五十周岁的男性Sprague-Dawley大鼠。还有10只大鼠的对照组(Chow对照组),而另一只大鼠的高脂饮食喂食八周以诱导肥胖症。然后将大鼠分配到四个随机组中。将大鼠每天溶解在1ml无菌蒸馏水中的10mg / kg氯化锂(LICL),每周5次。大鼠进行了20分钟的跑步机行走,运动强度为40%最大氧吸收(VO 2 MAX)(12米/分钟,斜率0%)。这是每天3天的每天20分钟进行。在肥胖大鼠中,12周的锂治疗或耐久性运动明显减少体重和体脂肿块,而不显示在丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平的平行或显着的毒性反应中的含有或显着的毒性反应时的添加剂效应和肾脏和肝组织。在运动和锂基团中,海马中的BDNF表达显着增加,其中在该组中发现了协同作用,其中运动和锂处理都是平行的。另一方面,仅在锂处理组中显示GSK3β活性的降低,而不显示在处理处理时的添加剂效应。锂电片和低强度耐久性锻炼12周增加了BDNF的表达,肥胖小鼠海马的神经保护剂。单独锂处理抑制GSK3β的活性。这可以被解释为两种因素在预防神经变性疾病中的适用性的积极迹象。

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