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Xiaorong Yang [1] and Peipei Si [1; 2] and Huaping Qin [1] and Litian Yin [1] and Liang-Jun Yan [3] and Ce Zhang [1]

Academic Editor: Javier Egea

1, National Key Disciplines, Key Laboratory for Cellular Physiology of Ministry of Education, Department of Neurobiology, Shanxi Medical University, No. 56 Xin Jian South Road, Taiyuan, 030001 Shanxi, China, sxmu.edu.cn

2, Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, 050071 Hebei, China, hebmu.edu.cn

3, Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA, unthsc.edu

Received Mar 29, 2017; Revised Jun 22, 2017; Accepted Jul 5, 2017

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.

1. Introduction

Silent information regulator 1 (SIRT1), an NAD+-dependent deacetylase, is known to deacetylate histone and nonhistone proteins such as transcription factors. It participates in a variety of physiopathological processes such as health maintenance in development, gametogenesis, homeostasis, longevity, and several neurodegenerative diseases as well as age-related disorders [1–5]. Recently, the neuroprotective effects of SIRT1 have attracted great interest. It has been found that SIRT1 could be upregulated to antagonize neuronal injury in different animal models, such as cerebral ischemia, Alzheimer’s disease (AD), and Huntington’s disease (HD) [6]. It has also been demonstrated that SIRT1 deacetylates p53, PGC-1α, and NF-κB to prevent many pathogenic processes. However, it remains unknown whether SIRT1 protects neurons from NMDA-mediated neurotoxicity in different excitotoxic insult models.

Glutamate is a primary excitatory amino acid neurotransmitter and activation of glutamate receptors including NMDA receptor plays crucial roles in the central nervous system. However, overactivation of NMDA receptor may cause intracellular calcium overload, leading to an enzymatic cascade of events resulting ultimately in cell death known as excitotoxicity [7]. A wide range of acute and chronic brain injury diseases, such as stroke/ischemia and epilepsy, and certain neurodegenerative disorders have been linked to NMDA receptor-mediated excitotoxicity [8]. Therefore, NMDA-induced excitotoxicity is a useful tool to evaluate neurotoxicity in isolated cells and is a good model of nerve injury that mimics closely the situation in vivo

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