Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/61448
Title: Gartanin protects neurons against glutamate-induced cell death in HT22 Cells : independence of Nrf-2 but involvement of HO-1 and AMPK
Authors: Gao, XY
Wang, SN
Yang, XH
Lan, WJ
Chen, ZW
Chen, JK
Xie, JH
Han, YF 
Pi, RB
Yang, XB
Keywords: AMP-activated protein kinase
Gartanin
Heme oxygenase 1
Neuroprotective
Nuclear factor erythroid-derived 2-like 2
Oxidative stress
Issue Date: 2016
Publisher: Springer
Source: Neurochemical research, 2016, v. 41, no. 9, p. 2267-2277 How to cite?
Journal: Neurochemical research 
Abstract: Oxidative stress mediates the pathogenesis of neurodegenerative disorders. Gartanin, a natural xanthone of mangosteen, possesses multipharmacological activities. Herein, the neuroprotection capacity of gartanin against glutamate-induced damage in HT22 cells and its possible mechanism(s) were investigated for the first time. Glutamate resulted in cell death in a dose-dependent manner and supplementation of 1–10 µM gartanin prevented the detrimental effects of glutamate on cell survival. Additional investigations on the underlying mechanisms suggested that gartanin could effectively reduce glutamate-induced intracellular ROS generation and mitochondrial depolarization. We further found that gartanin induced HO-1 expression independent of nuclear factor erythroid-derived 2-like 2 (Nrf2). Subsequent studies revealed that the inhibitory effects of gartanin on glutamate-induced apoptosis were partially blocked by small interfering RNA-mediated knockdown of HO-1. Finally, the protein expression of phosphorylation of AMP-activated protein kinase (AMPK) and its downstream signal molecules, Sirtuin activator (SIRT1) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), increased after gartanin treatment. Taken together, these findings suggest gartanin is a potential neuroprotective agent against glutamate-induced oxidative injury partially through increasing Nrf-2-independed HO-1 and AMPK/SIRT1/PGC-1α signaling pathways.
URI: http://hdl.handle.net/10397/61448
ISSN: 0364-3190 (print)
1573-6903 (online)
DOI: 10.1007/s11064-016-1941-x
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