Myocardial mitochondrial oxidative stress and dysfunction in intense exercise: regulatory effects of quercetin
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  • 作者:Chao Gao (1)
    Xiaoqian Chen (2)
    Juan Li (1)
    Yanyan Li (1)
    Yuhan Tang (1)
    Liang Liu (1)
    Shaodan Chen (1)
    Haiyan Yu (1)
    Liegang Liu (1)
    Ping Yao (1)
  • 关键词:Quercetin ; Exercise ; Oxidative stress ; Mitochondria
  • 刊名:European Journal of Applied Physiology
  • 出版年:2014
  • 出版时间:April 2014
  • 年:2014
  • 卷:114
  • 期:4
  • 页码:695-705
  • 全文大小:700 KB
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  • 作者单位:Chao Gao (1)
    Xiaoqian Chen (2)
    Juan Li (1)
    Yanyan Li (1)
    Yuhan Tang (1)
    Liang Liu (1)
    Shaodan Chen (1)
    Haiyan Yu (1)
    Liegang Liu (1)
    Ping Yao (1)

    1. Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Ministry of Education Key Laboratory of Environment, Ministry of Environmental Protection Key Laboratory of Environment, and Health (Wuhan) and State Key Laboratory of Environment Health (Incubation), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, People’s Republic of China
    2. Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, People’s Republic of China
  • ISSN:1439-6327
文摘
Introduction Oxidative stress plays a pivotal role in the intense exercise-induced myocardium injury, and mitochondrial compartment is presumed as the main source and susceptible target of intracellular reactive oxygen species (ROS). Purpose The objective of this study was to evaluate the protective effect of quercetin, a naturally occurring flavonoids possessing antioxidant effect on repeated intense exercise-induced mitochondrial oxidative stress and dysfunction. Methods Adult male BALB/C mice were treated by quercetin (100?mg/kg bw) for 4?weeks and subjected to the exercise protocol on a treadmill (28?m/min at 5° slope for 90?min) for seven consecutive days concurrently at the fourth week. Results Intense exercise in mice resulted in the leakage of creatine kinase-MB (increased from 221.5?±?33.8 to 151.1?±?19.1?U/l, P?<?0.01) and ultrastructural malformation mainly evidenced by disrupted myofibrils and swollen mitochondria, which was overtly attenuated by quercetin prophylaxis. Quercetin pretreatment evidently alleviated mitochondrial oxidative stress by inhibiting glutathione depletion and aconitase inactivation, ROS over-generation, and lipid peroxidation in cardiac mitochondria of intense exercise mice. Furthermore, mitochondrial dysfunction manifested by decreased mitochondrial membrane potential (68.6?±?7.6 versus 100.0?±?7.7?%, P?<?0.01) and respiratory control ratio (5.03?±?0.55 versus 7.48?±?0.71, P?<?0.01) induced as a consequence of acute exercise was markedly mitigated by quercetin precondition. Conclusion Quercetin protects mouse myocardium against intense exercise injury, especially ultrastructural damage and mitochondrial dysfunction, probably through its beneficial antioxidative effect, highlighting a promising strategy for over-training injury by naturally occurring phytochemicals.

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