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Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 150617, 9 pages
http://dx.doi.org/10.1155/2014/150617
Research Article

Mulberry Extracts Alleviate Aβ25–35-Induced Injury and Change the Gene Expression Profile in PC12 Cells

1Department of Nutrition, Tianjin Institute of Health and Environmental Medicine, Tianjin 300050, China
2Comparative Medicine Center, Institute of Laboratory Animal Science, Peking Union Medical College (PUMC) and Chinese Academy of Medical Sciences (CAMS), Beijing 100021, China
3Tianjin Agricultural College, 22 Jinjing Highway, Tianjin 300384, China
4Center for Disease Control and Prevention, PLA Chengdu Military Area Command, Chengdu 610021, China
5Department of Preventive Medicine, Hangzhou Normal University, Hangzhou 311121, China

Received 9 July 2014; Revised 27 October 2014; Accepted 28 October 2014; Published 17 December 2014

Academic Editor: Cheorl-Ho Kim

Copyright © 2014 Nan Song 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

Mulberry, which contained high amounts of anthocyanins, has been used in traditional Chinese medicine. Mulberry fruit extracts (ME) have demonstrated the antioxidant activity and neuroprotection. The study was to investigate the neuroprotective efficacy of ME against β-amyloid 25–35- (Aβ25–35-) induced PC12 cells injury. Cells preincubated with or without ME (200 μg/mL) for 24 h were treated with Aβ25–35 (20 μmol/L) for another 24 h. Cell viability was assessed by MTT, gene expression profiles were examined by cDNA microarrays, and RT-PCR were used to confirm the results of microarray assays. ME pretreatment was found to neutralize the cytotoxicity and prevent Aβ25–35-induced cells injury. Analyses of gene expression profile revealed that genes involving cell adhesion, peptidase activity, cytokine activity, ion binding activity, and angiogenesis regulation were significantly modulated by ME pretreatment. Among those genes, Apaf1, Bace2, and Plcb4 were enriched in the “Alzheimer’s disease-reference pathway” and downregulated after ME intervention. RT-PCR results showed that ME preincubation could significantly inhibit Aβ25–35 increased mRNA levels of these three genes. Overall, ME pretreatment could substantially alleviate PC12 cells injury and downregulate expression of AD-related genes, such as Apaf1, Bace2, and Plcb4. This study has a great nutrigenomics interest and brings new and important light in the field of AD intervention.