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CJAP ›› 2016, Vol. 32 ›› Issue (3): 260-263.doi: 10.13459/j.cnki.cjap.2016.03.018

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The changes of HIF-1α and AMPKα2 expression levels during skeletal muscle blunt injury recovery

WEN Han1, GE Xin-fa1,2, DONG Gui-jun2, PANG Hong-bo3, ZHANG Li-hui4   

  1. 1. Shanghai University of Sport, Shanghai 200438;
    2. Shandong Spot University, Jinan 250102;
    3. Tianjin Disabled Rehabilitation Center, Tianjin 300381;
    4. Qinhuangdao Port Hospital of Hebei Port Group Co., Ltd, Qinhuangdao 066002, China
  • Received:2015-11-13 Revised:2016-02-14 Online:2016-05-28 Published:2018-06-12
  • Supported by:

Abstract: Objective:To explore the possible biological mechanisms of skeletal muscle injury recovery by observing the changes of AMP-activated protein kinase α2 (AMPKα2) and hypoxia inducible factor-1α (HIF-1α) expression levels of rats in the skeletal muscle blunt injury recovery process. Method:Six of the 48 male Wistar rats was randomly selected as the normal control group. The blunt injury model was set up by injuring the hind legs of remaining 42 rats with heavy objects. Then they were divided into 7 groups (n=6). The changes of AMPKα2 and HIF-1α expression levels were tested in the hind limb triceps surae of the model rats from each of the 7 groups at 12 hours, 2 days, 5 days, 7 days, 10 days, 15 days and 30 days respectively following the injury. Results:The expression levels of AMPKα2 and HIF-1α all increased significantly at 12 hours following the injury and fell close to normal levels at 15 days following the injury. The values of AMPKα2 and HIF-1α expression peaked within 2 days after injury and the expression levels began to decline at 5 days after injury. Except the peak, the changes of the mRNA expressions of the two proteins were basically consistent with those of protein expression at the other time points. Conclusion:HIF-1α and AMPKα2 might play roles in mediating hypoxia adaptation, muscle cell regeneration, and energy compensation to promote recovery after injury.

Key words: skeletal muscle blunt injury, AMPKα2, HIF-1a, mitochondrial autophagy, the energy compensation, mouse

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