Please use this identifier to cite or link to this item: http://repo.knmu.edu.ua/handle/123456789/22147
Title: Oral consumption of caffeinated energy drinks increases expression of Ki-67 but decreases brain-derived neurotrophic factor in the brain of rats
Authors: Tkachenko, Anton
Gubina-Vakulyck, Galina
Onishchenko, Anatolii
Gorbach, Tetiana
Nakonechna, Oksana
Kufterina, Nataliya
Shekhovtsova, E.
Tkachenko, M.
Keywords: brain-derived neurotrophic factor
β-Nerve Growth Factor
caffeine
energy drinks
Ki-67 Antigen
Issue Date: 12-Oct-2018
Citation: Oral consumption of caffeinated energy drinks increases expression of Ki-67 but decreases brain-derived neurotrophic factor in the brain of rats / A. S. Tkachenko, G. I. Gubina-Vakulyck, A. I. Onishchenko, T. V. Gorbach, O. A. Nakonechna, N. S. Kufterina, E. V. Shekhovtsova, M. O. Tkachenko // Brunei International Medical Journal. – 2018. – Vol. 14. – P. 140–146.
Abstract: Cytotoxic effects of caffeinated energy drinks and their components have previously been reported. The aim of this study was to investigate the effect of regular oral consumption of caffein-ated energy drinks on the brain, especially on cerebral Ki-67 expression, levels of brain-derived neu-rotrophic factors and β-nerve growth factor in a rat model. Materials and methods. The brain ho-mogenate levels of BDNF and β-NGF were measured in rats fed on a regular diet of caffeinated ener-gy drinks for two months, using commercially available ELISA kits and compared with levels meas-ured in control rats. Ki-67 expression was assessed immunohistochemically to evaluate the prolifera-tion rate of different types of cells in the brain tissue. Results. Caffeinated energy drink consumption for two months was associated with the development of histological features of brain edema, signifi-cantly increased expression of Ki-67 with BDNF levels significantly reduced by half (p=0.02), in brain homogenates compared to control rats. Conclusions. Chronic oral consumption of caffeinated energy drinks was associated with significantly reduced BDNF levels and an overexpression of Ki-67 in mac-roglial cells, endotheliocytes, and ventricular ependymocytes suggesting a proliferative response to neural injury.
URI: https://repo.knmu.edu.ua/handle/123456789/22147
Appears in Collections:Наукові праці. Кафедра біологічної хімії

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