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The Journal of Exercise Nutrition & Biochemistry
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eISSN : 2233-6842

Special Article

pISSN : 2233-6834
eISSN : 2233-6842
Editor in Chief : Jonghoon Park
The Journal of Exercise Nutrition & Biochemistry - Vol. 23 , No. 4

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

Jisu Kim / Kang Pa Lee / Suji Beak / Hye Ra Kang / Yong Kyun Kim / Kiwon Lim

[Figure] Transcriptomic profiles and cell viability in response to BCE treatment in A棺-induced primary neuron cell death. (A) Hierarchical clustering of microarray data obtained from BCE-treated (with 300 關g/mL) amyloid beta (A棺)-stimulated primary neuronal cells. (B) The primary neuronal cells (1 횞 105) were treated with A棺 25-35 (20 uM), with or without BCE (300 關g/mL) for 24 h. Bar graphs indicate the percentage of cell viability. Data are expressed as the mean 짹 SE values from three independent experiments. *P < 0.05 compared to only A棺 25-35 treated group. (C) The Live/Dead cell reagents were dispensed into each well, and these images were acquired using a fluorescence microscope (excitation 580 nm and emission 604 nm). Un: untreated group; BCE: black chokeberry ethanol extract treated group; A棺: amyloid 棺 treated group

[Purpose] Numerous epidemiological studies have shown that it is possible to prescribe exercise for neurodegenerative disease, such as Alzheimer's disease and Parkinson셲 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-1慣, 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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