Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ejphar.2009.07.017
Title: Inhibition of H2O2-induced neuroblastoma cell cytotoxicity by a triazine derivative, AA3E2
Authors: Shaykhalishahi, H.
Yazdanparast, R.
Ha, H.-H. 
Chang, Y.-T. 
Keywords: Alzheimer's disease
Antioxidant
Apoptosis
Hydrogen peroxide
SK-N-MC cell
Triazine compound
Issue Date: 10-Nov-2009
Source: Shaykhalishahi, H., Yazdanparast, R., Ha, H.-H., Chang, Y.-T. (2009-11-10). Inhibition of H2O2-induced neuroblastoma cell cytotoxicity by a triazine derivative, AA3E2. European Journal of Pharmacology 622 (1-3) : 1-6. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ejphar.2009.07.017
Abstract: Alzheimer's disease is the major cause of senile dementia with the hallmark of β-amyloid deposition in neurons. Although the main cause(s) of this deposition is not fully understood, however, the wealth of the present literature data supports the pivotal role of reactive oxygen and nitrogen species in both the initiation and progression of β-amyloid aggregation and deposition. In the present study, we were interested to evaluate the free-radical protecting effect of AA3E2, a triazine derivative with a β-amyloid-breaking activity, among SK-N-MC neuroblastoma cells exposed to hydrogen peroxide (H2O2) as an exogenous source of free radicals. Exposure of the cells to different doses of AA3E2 (1-16 μM) for 3 h followed by subsequent exposure to a single dose of H2O2 (mainly 150 μM) attenuated the extent of superoxide dismutase (SOD) and catalase (CAT) inhibition by H2O2, in a dose dependent manner. Furthermore, significant reduction was observed in the extent of cellular lactate dehydrogenase release, intracellular ROS and the extent of apoptosis among the cells pre-treated with AA3E2. Based on these data, an antioxidant mode of action is proposed for AA3E2 besides its previously β-amyloid-breaking activity. © 2009 Elsevier B.V. All rights reserved.
Source Title: European Journal of Pharmacology
URI: http://scholarbank.nus.edu.sg/handle/10635/94052
ISSN: 00142999
DOI: 10.1016/j.ejphar.2009.07.017
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