摘要
目的:研究低氧和低氧训练对AMPKα2转基因小鼠骨骼肌CPT-1的mRNA和蛋白表达水平的影响,进而探讨低氧和低氧训练中AMPKα2调节脂肪酸氧化过程的可能机制。方法:健康两月龄C57BL/6J品系的野生小鼠和AMPKα2转基因小鼠,分别分为常氧安静组、低氧安静组和低氧训练组,共六组,每组10只。低氧组小鼠持续暴露于低氧房中(模拟海拔4000m高度,氧浓度12.3%),其中低氧训练组小鼠还要在此低氧房中进行跑台运动,12m/min,每天1h,持续2周。测定股四头肌AMPKα2蛋白水平以及CPT-1的mRNA和蛋白表达情况。结果:2周的低氧和低氧训练对AMPKα2的蛋白表达没有显著的影响;低氧和低氧训练均显著提高了CPT-1的mRNA表达(P<0.05);低氧对野生和AMPKα2转基因小鼠CPT-1的作用无差异;低氧训练组中,AMPKα2转基因小鼠的CPT-1 mRNA表达显著高于野生小鼠(P<0.05),与低氧安静组相比,低氧训练使转基因小鼠的CPT-1蛋白表达产生了显著增加(P<0.05),但是野生小鼠并无显著变化。结论:AMPKα2参与调节了低氧训练中骨骼肌CPT-1的表达水平,促进脂肪酸的氧化过程。
Objective: To study the effects of hypoxia and hypoxia training on the expressions of CPT-1 mRNA and protein in AMPKα2 transgenic mice skeletal muscle.Furthermore,we explore the possible mechanism of AMPKα2 in regulating fatty acid oxidation during hypoxia and hypoxia training.Methods: Healthy C57BL/6J wild-type(WT) mice and AMPKα2 transgenic(TG) mice,two months old,were randomly divided into control groups,hypoxia groups and hypoxia training groups each.Hypoxia groups and hypoxia training groups were exposed in the hypoxia room the whole day for two weeks(simulation of 4000m altitude,oxygen concentration 12.3%),and meanwhile hypoxia training groups were trained to run on the treadmill(12 m/min,1h/day).After that,quadriceps femoris muscle were removed,and then the expression of AMPKα2 protein and CPT-1 mRNA and protein were measured.Results: Either hypoxia or hypoxia training had no effect on the expression of AMPKα2 protein;both hypoxia and hypoxia training significantly increased CPT-1 mRNA expression(P0.05);in hypoxia groups,there was no apparent difference in CPT-1 expression between WT and TG mice;after two weeks hypoxia training,the expression of CPT-1 mRNA of TG mice was significantly higher than that of WT mice(P0.05) and compared with hypoxia groups,the expression of CPT-1 protein of TG mice was higher in hypoxia training groups(P0.05),but hypoxia training didn't change that of WT mice.Conclusion: During hypoxia training,AMPKα2 is activated to regulate the expression level of CPT-1 in skeletal muscle,so that it stimulates fatty acid oxidation.
出处
《北京体育大学学报》
CSSCI
北大核心
2011年第1期51-53,57,共4页
Journal of Beijing Sport University
基金
北京市自然科学基金(5072031)
卫生部人类疾病比较医学重点实验室开放课题基金(ZDS200804)