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Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 7480980, 10 pages
Research Article

A Chinese Herbal Formula, Gengnianchun, Ameliorates β-Amyloid Peptide Toxicity in a Caenorhabditis elegans Model of Alzheimer’s Disease

1Department of Gynecology, The First Hospital of Jilin University, Changchun, China
2Department of Integrated Traditional Chinese Medicine and Western Medicine, Obstetrical and Gynecological Hospital, Fudan University, Shanghai, China

Correspondence should be addressed to Wenjun Wang; moc.361@36gnawnujnew and Yan Fu; nc.ude.ulj@y_f

Received 26 April 2017; Revised 26 August 2017; Accepted 7 September 2017; Published 11 October 2017

Academic Editor: Louise Bennett

Copyright © 2017 Fanhui Meng 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.


Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, and the few drugs that are currently available only treat the symptoms. Traditional medicine or phytotherapy has been shown to protect against AD. In our previous studies, Gengnianchun (GNC), a traditional Chinese medicine formula with a prolongevity effect, protected against Aβ-induced cytotoxicity in pheochromocytoma cells (PC-12 cells) and hippocampal cells. Here, we investigated the effects and possible mechanisms by which GNC protected against Aβ toxicity using transgenic Caenorhabditis elegans CL4176. Our results showed that GNC effectively delayed the Aβ toxicity-triggered body paralysis of CL4176 worms. GNC decreased Aβ by reducing Aβ mRNA levels. Moreover, GNC significantly reduced reactive oxygen species in the AD model worms compared with the controls. In addition, GNC upregulated the daf-16, sod-3, hsp-16.2 genes, and enhanced DAF-16 translocation from the cytoplasm to the nuclei under oxidative stress conditions. GNC treatment of C. elegans strains lacking DAF-16 did not affect the paralysis phenotype. Taken together, these findings suggest that GNC could protect against Aβ-induced toxicity via the DAF-16 pathway in C. elegans. Further studies are required to analyze its effectiveness in more complex animals.