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Effect of black chokeberry on skeletal muscle damage and neuronal cell death

  • Kim, Jisu (Department of Sports Medicine and Science in Graduated School, Konkuk University) ;
  • Lee, Kang Pa (Department of Bio-Science, College of Natural Science, Dongguk University) ;
  • Beak, Suji (Department of Bio-Science, College of Natural Science, Dongguk University) ;
  • Kang, Hye Ra (Department of Radiological Science, Daewon University college) ;
  • Kim, Yong Kyun (Department of Radiological Science, Daewon University college) ;
  • Lim, Kiwon (Department of Sports Medicine and Science in Graduated School, Konkuk University)
  • Received : 2019.12.03
  • Accepted : 2019.12.13
  • Published : 2019.12.31

Abstract

[Purpose] Numerous epidemiological studies have shown that it is possible to prescribe exercise for neurodegenerative disease, such as Alzheimer's disease and Parkinson's disease. However, despite the availability of diverse scientific knowledge, the effects of exercise in this regard are still unclear. Therefore, this study attempted to investigate a substance, such as black chokeberry (Aronia melanocapa L.) that could improve the ability of the treatment and enhance the benefits of exercising in neurodegenerative diseases. [Methods] The cell viability was tested with 2,3-bis[2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolim-5-carboxanilide and the cells were stained with ethidium homodimer-1 solution. The mRNA expression levels were evaluated by microarray. The active compounds of black chokeberry ethanolic extract (BCE) were analyzed by gas chromatography. The chemical shift analysis in the brain was performed using magnetic resonance spectroscopy. [Results] BCE treatment decreased hydrogen peroxide-induced L6 cell death and beta amyloid induced primary neuronal cell death. Furthermore, BCE treatment significantly reduced the mRNA levels of the inflammatory factors, such as IL-1α, Cxcl13, IL36rn, Itgb2, Epha2, Slamf8, Itgb6, Kdm6b, Acvr1, Cd6, Adora3, Cd27, Gata3, Tnfrsf25, Cd40lg, Clec10a, and Slc11a1, in the primary neuronal cells. Next, we identified 16 active compounds from BCE, including D-mannitol. In vivo, BCE (administered orally at a dosage of 50 mg/kg) significantly regulated chemical shift in the brain. [Conclusion] Our findings suggest that BCE can serve as a candidate for neurodegenerative disease therapy owing to its cyto-protective and anti-inflammatory effects. Therefore, BCE treatment is expected to prevent damage to the muscles and neurons of the athletes who continue high intensity exercise. In future studies, it would be necessary to elucidate the effects of combined BCE intake and exercise.

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Acknowledgement

This paper was supported by the KU Research Professor Program of the Konkuk University. The authors declare that there is no conflict of interest regarding the publication of this article.