Effect of exercise preconditioning on mitochondrial biogenesis in rat hippocampus after acute hypobaric hypoxia
LIU Jing1, ZHANG Hongying2, BO Hai3, KANG Weimin4
1.Department of Pathology, the Third Medical Center of PLA General Hospital, Beijing 100039, China; 2.Department of Quality Management, the Third Medical Center of PLA General Hospital, Beijing 100039, China; 3. Department of Military Training Medicine, Logistics University of PAPF, Tianjin 300309, China; 4. Stroke Medical Therapeutic Center, the General Hospital of PLA Rocket Force, Beijing 100032, China
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.
刘静, 张红英, 薄海, 康伟民. 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[J]. 武警医学, 2019, 30(11): 932-935.
LIU Jing, ZHANG Hongying, BO Hai, KANG Weimin. Effect of exercise preconditioning on mitochondrial biogenesis in rat hippocampus after acute hypobaric hypoxia. Med. J. Chin. Peop. Armed Poli. Forc., 2019, 30(11): 932-935.
Czerniczyniec A, La P P, Bustamante J, et al. Mitochondrial function in rat cerebral cortex and hippocampus after short- and long-term hypobaric hypoxia[J]. Brain Res, 2015, 1598: 66-75.
[3]
Ploumi C, Daskalaki I, Tavernarakis N. Mitochondrial biogenesis and clearance: a balancing act[J]. FEBS J, 2017, 284(2): 183-195.
Bo H, Kang W, Jiang N, et al. Exercise-induced neuroprotection of hippocampus in APP/PS1 transgenic mice via upregulation of mitochondrial 8-oxoguanine DNA glycosylase[J]. Oxid Med Cell Longev, 2014,7(6):834502.
[6]
Pires J, Haynes C M. Mitochondrial biogenesis: MitoCPR resuscitates import-defective mitochondria[J]. Curr Biol, 2018, 28(11):669-671.
[7]
Pialoux V, Mounier R. Hypoxia-induced oxidative stress in health disorders[J]. Oxid Med Cell Longev, 2012,5(6): 940121.
[8]
Niemann J, Johne C, Schroder S, et al. An mtDNA mutation accelerates liver aging by interfering with the ROS response and mitochondrial life cycle [J]. Free Radic Biol Med, 2017, 102: 174-187.
[9]
Islam H, Edgett B A, Gurd B J. Coordination of mitochondrial biogenesis by PGC-1alpha in human skeletal muscle: A re-evaluation[J]. Metabolism, 2018, 79: 42-51.
[10]
Andrabi S S, Parvez S, Tabassum H. Progesterone induces neuroprotection following reperfusion-promoted mitochondrial dysfunction after focal cerebral ischemia in rats[J]. Dis Model Mech, 2017, 10(6): 787-796.
[11]
Zhang X M, Zhang L, Wang G, et al. Suppression of mitochondrial fission in experimental cerebral ischemia: the potential neuroprotective target of p38 MAPK inhibition[J]. Neurochem Int, 2015,36(6):1-8.
Belviranli M, Okudan N. Exercise training protects against aging induced cognitive dysfunction via activation of the hippocampal PGC-1alpha/FNDC5/BDNF pathway.[J]. Neuromolecular Med, 2018, 20(3): 386-400.
[14]
Zhang L, He Z, Zhang Q, et al. Exercise pretreatment promotes mitochondrial dynamic protein OPA1 expression after cerebral ischemia in rats[J]. Int J Mol Sci, 2014, 15(3): 4453-4463.
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