目的 探讨运动预适应对急性低压低氧大鼠脑海马线粒体生物合成影响。方法 大鼠分为对照组(normal control group, NC)、急性低氧组(acute hypoxia group, AH)和运动预适应(exercise preconditioning,EP)联合急性低氧组(acute hypoxia group,AH),每组8只。EP联合AH组大鼠在常氧环境进行6周跑台训练,坡度5°, 速度17 m/min,60 min/d,5次/周。AH组和EP+AH大鼠置于低压低氧舱8 h,压力0.06 MPa,氧含量10%±2%。荧光定量PCR法检测mtDNA拷贝数,荧光探针法检测线粒体膜电位,ROS生成速率和ATP合成活力,Western blotting 检测PGC-1α、NRF-1和Tfam蛋白表达。结果 AH组大鼠脑海马mtDNA拷贝数为1.69±0.20,较NC组(1.00±0.13)明显增高;线粒体ROS产生速率为(9.49±1.25) pmol/(min·mg protein),较NC组值(4.83±0.66) pmol/(min·mg protein)明显增高;PGC-1α蛋白表达量为(189.24±21.77),较NC组(100.00±12.90)明显增高;线粒体膜电位为(4.51±0.65),较NC组(8.27±1.02)明显降低;差异均具有统计学意义(P＜0.05)。EP+AH组大鼠脑海马mtDNA拷贝数为(1.19±0.15),较AH组(1.69±0.20)明显降低;线粒体ROS产生速率为(6.01±0.93) pmol/(min·mg protein),较AH组值(9.49±1.25) pmol/(min·mg protein)明显降低;PGC-1α蛋白表达量为141.95±18.12,较AH组(189.24±21.77)明显降低;线粒体膜电位为(7.02±1.10),较AH组(4.51±0.65)明显升高;上述差异均具有统计学意义(P＜0.05)。结论 运动预适应可抑制急性低压低氧对线粒体生物合成的上调效应,同时改善线粒体能量代谢能力,抑制氧化应激。
Abstract
Objective To investigate the effect of exercise preconditioning on mitochondrial biogenesis in the rat hippocampus after acute hypobaric hypoxia.Methods Rats were randomly divided into three groups: normal control group (NC), acute hypoxia group (AH), and exercise preconditioning+ acute hypoxia group (EP+AH). Rats in the EP+AH group underwent six weeks of treadmill training on the plain at a speed of 17 m/min, -5° grade for 60 min/day. Rats in AH and EP+AH groups were placed in a hypobaric hypoxia chamber at 0.06 MPa pressure and 10%±2% oxygen for 8 consecutive hours. The mtDNA copies, mitochondrial membrane potential, ROS generation rate, ATP synthesis activity, and the protein expression of PGC-1α, NRF-1, Tfam were measured.Results The mtDNA copies, ROS generation rate, PGC-1αprotein expression, and mitochondrial membrane potential in the AH group were 1.69±0.20, (9.49±1.25) pmol/(min·mg protein), 189.24±21.77, and 4.51±0.65 respectively, compared with 1.00±0.13, (4.83±0.66) pmol/(min·mg protein), 100.00±12.90, and 8.27±1.02 in the NC group respectively. The difference was statistically significant (P＜0.05 or P＜0.01) . The mtDNA copies, ROS generation rate, PGC-1αprotein expression, and mitochondrial membrane potential in the EP+AH group were 1.19±0.15, (6.01±0.93) pmol/(min·mg protein), 141.95±18.12, and 7.02±1.10, respectively, compared with 1.69±0.20, (9.49±1.25) pmol/(min·mg protein), 189.24±21.77, and 4.51±0.65 in the AH group respectively. The difference was also statistically significant (P＜0.05).Conclusions Exercise preconditioning can inhibit acute hypobaric hypoxia induced by mitochondrial biogenesis and oxidative stress while improving mitochondrial energy metabolism in the hippocampus.
关键词
运动预适应 /
低氧 /
脑海马 /
线粒体生物合成 /
能量代谢
Key words
exercise preconditioning /
hypoxia /
hippocampus /
mitochondrial biogenesis /
energy metabolism
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