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Stem Cells International
Volume 2016, Article ID 7419389, 9 pages
http://dx.doi.org/10.1155/2016/7419389
Research Article

N-Stearoyl-L-Tyrosine Inhibits the Senescence of Neural Stem/Progenitor Cells Induced by Aβ1–42 via the CB2 Receptor

1School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China
2Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Received 25 August 2015; Revised 16 November 2015; Accepted 1 December 2015

Academic Editor: Gary E. Lyons

Copyright © 2016 Wen-Qing Li 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

Alzheimer’s disease, one of the neurodegenerative diseases, shows the progressive senescence of neural progenitor/stem cells. N-Stearoyl-L-tyrosine (NsTyr) showed neuroprotective effect against chronic brain ischemia in previous reports. In the present study, we find the antisenescent effects of NsTyr-2K in NSPCs induced by A in vitro. Cell viability of NSPCs was evaluated by CCK8 assay; SA-β-gal staining was used to evaluate senescence of NSPCs. CB receptors were detected by immunohistochemistry in NSPCs. AM251 or AM630 was used to offset the anti-senescence effects afforded by NsTyr-2K. The positive rate of SA-β-gal staining was significantly increased in NSPCs after incubation with A for 9 days. CB receptors were found on the surface of NSPCs. The expression level of CB1 receptors was significantly decreased in NSPCs after incubation with A. This phenomenon was reversed dose-dependently by NsTyr-2K. NsTyr-2K attenuated A induced NSPCs senescence dose-dependently, and its antisenescence effect was completely abolished by AM630. A dose-dependently increased the prosenescence molecules p16 and Rb. Their expression was inhibited by NsTyr-2K dose-dependently and blocked by AM630 in NSPCs. These results suggest that NsTyr-2K can alleviate the senescence of NSPCs induced by A via CB2 receptor.