These authors contributed equally to this work.
Green tea epigallocatechin-3-gallate (EGCG) promotes neural progenitor cell proliferation and sonic hedgehog pathway activation during adult hippocampal neurogenesis
Article first published online: 13 JUN 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 56, Issue 8, pages 1292–1303, August 2012
How to Cite
Wang, Y., Li, M., Xu, X., Song, M., Tao, H. and Bai, Y. (2012), Green tea epigallocatechin-3-gallate (EGCG) promotes neural progenitor cell proliferation and sonic hedgehog pathway activation during adult hippocampal neurogenesis. Mol. Nutr. Food Res., 56: 1292–1303. doi: 10.1002/mnfr.201200035
- Issue published online: 10 AUG 2012
- Article first published online: 13 JUN 2012
- Manuscript Accepted: 20 APR 2012
- Manuscript Revised: 29 MAR 2012
- Manuscript Received: 26 JAN 2012
- National Natural Science Foundation of China. Grant Numbers: 30800441, 30972447
- Development and Regeneration Key Laboratory Foundation of Sichuan Province. Grant Number: SYS11-006
- Green tea;
- Learning and memory;
- Neural progenitor cell;
- Sonic hedgehog
Adult hippocampal neurogenesis is a lifelong feature of brain plasticity that appears to be critically involved in adult brain function and neurological disease. Recent studies suggest that (–)-epigallocatechin-3-gallate (EGCG), which is the main polyphenolic constituent of green tea, may be used for the prevention and treatment of various neurodegenerative diseases. We hypothesized that EGCG promotes adult neurogenesis, which may be beneficial to hippocampus-dependent learning and memory.
Methods and results
We show that EGCG treatment significantly increased the number of 5-bromo-2′-deoxyuridine (BrdU)-labeled cells in adult hippocampal neural progenitor cell (NPC) cultures and in the dentate gyrus of adult mice. Meanwhile, EGCG markedly improved spatial cognition in mice. These events are associated with the sonic hedgehog (Shh) signaling pathway. We observed that EGCG triggered a robust upregulation of Shh receptor (Patched) mRNA and protein expression in cultured NPCs as well as an upregulation of the downstream Shh transcriptional target Gli1. These changes were further confirmed in the hippocampus of mice administered EGCG. The blockage of the Shh signal with the pharmacological inhibitor cyclopamine attenuated EGCG-induced hippocampal neurogenesis.
Our results provide strong evidence that EGCG enhances adult hippocampal neurogenesis.