Table of Contents Author Guidelines Submit a Manuscript
Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 516741, 12 pages
http://dx.doi.org/10.1155/2013/516741
Research Article

The Aqueous Extract of Rhizome of Gastrodia elata Protected Drosophila and PC12 Cells against Beta-Amyloid-Induced Neurotoxicity

1Institute of Chinese Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
2State Key Laboratory of Phytochemistry & Plant Resources in West China, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
3School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
4School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong
5School of Life Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong

Received 7 June 2013; Accepted 30 July 2013

Academic Editor: Paul Siu-Po Ip

Copyright © 2013 Chun-Fai Ng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This study aims to investigate the neuroprotective effect of the rhizome of Gastrodia elata (GE) aqueous extract on beta-amyloid(Aβ)-induced toxicity in vivo and in vitro. Transgenic Drosophila mutants with Aβ-induced neurodegeneration in pan-neuron and ommatidia were used to determine the efficacy of GE. The antiapoptotic and antioxidative mechanisms of GE were also studied in Aβ-treated pheochromocytoma (PC12) cells. In vivo studies demonstrated that GE (5 mg/g Drosophila media)-treated Drosophila possessed a longer lifespan, better locomotor function, and less-degenerated ommatidia when compared with the Aβ-expressing control (all ). In vitro studies illustrated that GE increased the cell viability of Aβ-treated PC12 cells in dose-dependent manner, probably through attenuation of Aβ-induced oxidative and apoptotic stress. GE also significantly upregulated the enzymatic activities of catalase, superoxide dismutase, and glutathione peroxidase, leading to the decrease of reactive oxidation species production and apoptotic marker caspase-3 activity. In conclusion, our current data presented the first evidence that the aqueous extract of GE was capable of reducing the Aβ-induced neurodegeneration in Drosophila, possibly through inhibition of apoptosis and reduction of oxidative stress. GE aqueous extract could be developed as a promising herbal agent for neuroprotection and novel adjuvant therapies for Alzheimer’s disease.