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BioMed Research International
Volume 2015, Article ID 854359, 13 pages
http://dx.doi.org/10.1155/2015/854359
Research Article

The Protective Effect of Melatonin on Neural Stem Cell against LPS-Induced Inflammation

1Department of Anatomy, Yonsei University College of Medicine, Brain Korea 21 Project for Medical Science, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Republic of Korea
2BK21 Plus Project for Medical Sciences and Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea
3Department of Neurology, Seoul National University College of Medicine, Seoul 151-742, Republic of Korea

Received 10 August 2014; Revised 5 November 2014; Accepted 13 November 2014

Academic Editor: Janusz Blasiak

Copyright © 2015 Juhyun 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

Stem cell therapy for tissue regeneration has several limitations in the fact that transplanted cells could not survive for a long time. For solving these limitations, many studies have focused on the antioxidants to increase survival rate of neural stem cells (NSCs). Melatonin, an antioxidant synthesized in the pineal gland, plays multiple roles in various physiological mechanisms. Melatonin exerts neuroprotective effects in the central nervous system. To determine the effect of melatonin on NSCs which is in LPS-induced inflammatory stress state, we first investigated nitric oxide (NO) production and cytotoxicity using Griess reagent assays, LDH assay, and neurosphere counting. Also, we investigated the effect of melatonin on NSCs by measuring the mRNA levels of SOX2, TLX, and FGFR-2. In addition, western blot analyses were performed to examine the activation of PI3K/Akt/Nrf2 signaling in LPS-treated NSCs. In the present study, we suggested that melatonin inhibits NO production and protects NSCs against LPS-induced inflammatory stress. In addition, melatonin promoted the expression of SOX2 and activated the PI3K/Akt/Nrf2 signaling under LPS-induced inflammation condition. Based on our results, we conclude that melatonin may be an important factor for the survival and proliferation of NSCs in neuroinflammatory diseases.