运动预适应对急性低压低氧大鼠脑海马线粒体生物合成的影响

 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。

Effect of exercise preconditioning on mitochondrial biogenesis in rat hippocampus after acute hypobaric hypoxia

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.