Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/76389
Title: Indirubin-3-oxime prevents H2O2-induced neuronal apoptosis via concurrently inhibiting GSK3 beta and the ERK pathway
Authors: Yu, J
Zheng, JC
Lin, JJ
Jin, LL
Yu, R
Mak, SH 
Hu, SQ 
Sun, HY
Wu, X
Zhang, ZJ
Lee, M
Tsim, WK
Su, W
Zhou, WH
Cui, W
Han, YF 
Wang, QW
Keywords: Indirubin-3-oxime
H2O2
GSK3 beta
PI3-K
ERK
Issue Date: 2017
Publisher: Springer
Source: Cellular and molecular neurobiology, 2017, v. 37, no. 4, p. 655-664 How to cite?
Journal: Cellular and molecular neurobiology 
Abstract: Oxidative stress-induced neuronal apoptosis plays an important role in many neurodegenerative disorders. In this study, we have shown that indirubin-3-oxime, a derivative of indirubin originally designed for leukemia therapy, could prevent hydrogen peroxide (H2O2)-induced apoptosis in both SH-SY5Y cells and primary cerebellar granule neurons. H2O2 exposure led to the increased activities of glycogen synthase kinase 3 beta (GSK3 beta) and extracellular signal-regulated kinase (ERK) in SH-SY5Y cells. Indirubin-3-oxime treatment significantly reversed the altered activity of both the PI3-K/Akt/GSK3 beta cascade and the ERK pathway induced by H2O2. In addition, both GSK3 beta and mitogen-activated protein kinase inhibitors significantly prevented H2O2-induced neuronal apoptosis. Moreover, specific inhibitors of the phosphoinositide 3-kinase (PI3-K) abolished the neuroprotective effects of indirubin-3-oxime against H2O2-induced neuronal apoptosis. These results strongly suggest that indirubin-3-oxime prevents H2O2-induced apoptosis via concurrent inhibiting GSK3 beta and the ERK pathway in SH-SY5Y cells, providing support for the use of indirubin-3-oxime to treat neurodegenerative disorders caused or exacerbated by oxidative stress.
URI: http://hdl.handle.net/10397/76389
ISSN: 0272-4340
EISSN: 1573-6830
DOI: 10.1007/s10571-016-0402-z
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