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Open Journal of Neuroscience

ISSN: 2075-9088
Volume 5, 2017

Open Journal of Neuroscience, 2012, 2-1 [Research Article]

Theaflavins stimulate autophagic degradation of α-synuclein in neuronal cells

Kazunari Sekiyama1, Masaaki Nakai1,2, Masayo Fujita1, Takato Takenouchi3, Masaaki Waragai1, Jianshe Wei1, Akio Sekigawa1, Yoshiki Takamatsu1, Shuei Sugama4, Hiroshi Kitani3, Makoto Hashimoto1
1 Division of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Tokyo, 156-0057, Japan
2 Avian Influenza Research Center, Kyoto Sangyo University, Kyoto, Japan
3 Division of Animal Sciences, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8634, Japan
4 Department of Physiology, Nippon Medical School, Tokyo 113-8602, Japan

Corresponding Author & Address:

Makoto Hashimoto
Division of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Tokyo, 156-0057, Japan; E-mail: hashimoto-mk@igakuken.or.jp; Tel: +81-3-6834-2354; Fax: +81-3-5316-3150

Article History:
Published: 26th March, 2012   Accepted: 26th March, 2012
Received: 22nd December, 2011   Revised:  16th February, 2012

© Hashimoto et al.; licensee Ross Science Publishers

ROSS Open Access articles will be distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided that the original work will always be cited properly.

Keywords: Parkinson’s disease, theaflavin, autophagy, LC-3, α-synuclein


Given the recent epidemiological evidence showing an inverse correlation between black tea intake and the risk of Parkinson’s disease, it is an intriguing possibility that theaflavins, major natural polyphenols contained in black tea, may have an anti-neurodegenerative action. In this communication, we show that theaflavins act stimulatingly on autophagy in neuronal cells. Treatment of murine Neuro2A cells with theaflavin-3,3’-digallate (TF-3,3’) under the serum-free conditions resulted in stimulation of LC3-II expression and formation of LC3-positive, double-membrane autophagosomes. Under the same conditions, lysosomal activity was little affected by TF-3,3’, while the upregulation of LC3-II by TF-3,3’ was abrogated by 3-methyadenine treatment. Further studies revealed that TF-3,3’ might stimulate degradation of Akt at proteasome, leading to suppression of mTOR phosphorylation and enhancement of autophagy. Finally, expression of the transfected α-synuclein in these cells was significantly decreased by treatment with TF-3,3’. These results suggest that theaflavins’ autophagy-stimulating action might account for the prophylactic effects of black tea on Parkinson’s disease.

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