IMR Press / JIN / Volume 18 / Issue 4 / DOI: 10.31083/j.jin.2019.04.1174
Open Access Original Research
Diphenyleneiodonium chloride synergizes with diazoxide to enhance protection against amyloid β induced neurotoxicity
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1 Deparment of Neurology, Linyi People’s Hospital, Shandong Province, 276003, P. R. China
2 Central Laboratory, Linyi People’s Hospital, Shandong Province, 276003, P. R. China
3 Deparment of Neurology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, P. R. China
*Correspondence: (Quanping Su); (Guozhao Ma)
J. Integr. Neurosci. 2019, 18(4), 445–449;
Submitted: 2 September 2019 | Accepted: 28 November 2019 | Published: 30 December 2019
Copyright: © 2019 Fu et al. Published by IMR Press.
This is an open access article under the CC BY-NC 4.0 license

We examined synergistic effects of inhibiting reactive oxygen species generated from the mitochondria and from nicotinamide adenine dinucleotide phosphate oxidase on neurotoxicity. Primary hippocampal neurons were exposed to amyloid β, and the cells were treated with diazoxide or/and diphenyleneiodonium chloride. We found that the cell viability was decreased significantly after exposure to amyloid β for 72 h with higer reactive oxygen species and malondialdehyde levels, higher caspase-3 and cleaved caspase-3 levels and lower B-cell lymphoma 2 (Bcl-2) level. Both diazoxide and diphenyleneiodonium increased cell viability by inhibiting the increase in reactive oxygen species and caspase-3 activity as well as the decrease in Bcl-2 induced by amyloid β. The combination of diazoxide and diphenyleneiodonium exhibited better protective effects compared to a single treatment. In conclusion, the activation of a mitochondrial potassium channel in combination with the inhibitor of nicotinamide adenine dinucleotide phosphate oxidase exhibit synergistic protective effects against amyloid β neurotoxicity.

Alzheimer's disease
potassium channel
reactive oxygen species
Figure 1.
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