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Molecules 2014, 19(8), 10818-10831; https://doi.org/10.3390/molecules190810818

Cudarflavone B Provides Neuroprotection against Glutamate-Induced Mouse Hippocampal HT22 Cell Damage through the Nrf2 and PI3K/Akt Signaling Pathways

1
Inha Research Institute for Medical Sciences, Inha University School of Medicine, Incheon 400-712, Korea
2
College of Pharmacy, Wonkwang University, Iksan 570-749, Korea
3
College of Pharmacy, Keimyung University, 1095 Dalgubeol-daero, Daegu 704-701, Korea
*
Authors to whom correspondence should be addressed.
Received: 21 May 2014 / Revised: 10 July 2014 / Accepted: 15 July 2014 / Published: 24 July 2014
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Abstract

Oxidative cell damage contributes to neuronal degeneration in many central nervous system (CNS) diseases such as Alzheimer’s disease, Parkinson’s disease, and ischemia. Nrf2 signaling-mediated heme oxygenase (HO)-1 expression acts against oxidants that are thought to play a key role in the pathogenesis of neuronal diseases. Cudraflavone B is a prenylated flavone isolated from C. tricuspidata which has shown anti-proliferative activity, mouse brain monoamine oxidase (MAO) inhibitory effects, apoptotic actions in human gastric carcinoma cells and mouse melanoma cells, and hepatoprotective activity. In this study, cudraflavone B showed neuroprotective effects and reactive oxygen species (ROS) inhibition against glutamate-induced neurotoxicity by inducing the expression of HO-1 in mouse hippocampal HT22 cells. Furthermore, cudraflavone B caused the nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of antioxidant response elements (ARE) in mouse hippocampal HT22 cells. In addition, we found that the Nrf2-midiated HO-1 expression by cudraflavone B is involved in the cell protective response and ROS reductions, and cudraflavone B-induced expression of HO-1 was mediated through the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in HT22 cells. Our results demonstrated the potential application of naturally occurring cudraflavone B as a therapeutic agent from neurodegenerative disease. View Full-Text
Keywords: cudraflavone B; glutamate; oxidative stress; neuroprotection; mouse hippocampal HT22; nuclear factor-E2-related factor 2; heme oxygenase-1 cudraflavone B; glutamate; oxidative stress; neuroprotection; mouse hippocampal HT22; nuclear factor-E2-related factor 2; heme oxygenase-1
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Lee, D.-S.; Ko, W.; Kim, D.-C.; Kim, Y.-C.; Jeong, G.-S. Cudarflavone B Provides Neuroprotection against Glutamate-Induced Mouse Hippocampal HT22 Cell Damage through the Nrf2 and PI3K/Akt Signaling Pathways. Molecules 2014, 19, 10818-10831.

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