Anthocyanins Reversed D-Galactose-Induced Oxidative Stress and Neuroinflammation Mediated Cognitive Impairment in Adult Rats
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- 6 January 2016
- journal article
- research article
- Published by Springer Science and Business Media LLC in Molecular Neurobiology
- Vol. 54 (1), 255-271
- https://doi.org/10.1007/s12035-015-9604-5
Abstract
Aging is a major factor involved in neurological impairments, decreased anti-oxidant activities, and enhanced neuroinflammation. D-galactose (D-gal) has been considered an artificial aging model which induces oxidative stress and inflammatory response resulting in memory and synaptic dysfunction. Dietary supplementation exerts valuable effects against oxidative stress and neuroinflammation. Polyphenolic flavonoids, such as anthocyanins, have been reported as an anti-inflammatory and anti-oxidant agents against various neurodegenerative diseases. Recently, our group reported anthocyanin neuroprotection of the developing rat brain against ethanol-induced oxidative stress and neurodegenaration and ethanol-induced neuronal apoptosis via GABAB1 receptor intracellular signaling in prenatal rat hippocampus. Here, we examined the protective effect of anthocyanin neuroprotection against D-gal-induced oxidative and inflammatory response in the hippocampus and cortex regions and explore the potential mechanism of its action. Our results indicated that anthocyanins treatment significantly improved behavioral performance of D-gal-treated rats in Morris water maze and Y-maze tests. One of the potential mechanisms of this action was decreased expression of the receptor for advance glycation end product, reduced level of reactive oxygen species (ROS) and lipid peroxidation as well as markers of the Alzheimer’s disease. Furthermore, the results also indicated that anthocyanins inhibited activated astrocytes and neuroinflammation via suppression of various inflammatory markers including p-NF- K B, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNF-α) in the hippocampus and cortex regions of D-gal-treated rats brain. Moreover, anthocyanins abrogated neuroapoptosis via C-jun N-terminal kinase (p-JNK) suppression and improved deregulated synaptic proteins including synaptophysin, synaptosomal-associated protein (SNAP)-23, SNAP-25, and phosphorylated CREB. This data suggests that anthocyanins could be a safe and promising anti-oxidant and anti-neuroinflammatory agent for age-related neurodegenerative diseases such as Alzheimer’s disease.Keywords
Funding Information
- National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning ((2012-0009521).)
This publication has 81 references indexed in Scilit:
- Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation and neurodegeneration in the mouse hippocampusScientific Reports, 2015
- Ameliorative effect of black rice anthocyanin on senescent mice induced byd-galactoseFood & Function, 2014
- Protective effect of Millettia pulchra polysaccharide on cognitive impairment induced by d-galactose in miceCarbohydrate Polymers, 2014
- Advanced glycation endproducts and their receptor RAGE in Alzheimer's diseaseNeurobiology of Aging, 2009
- Soy isoflavones attenuate oxidative stress and improve parameters related to aging and Alzheimer’s disease in C57BL/6J mice treated with d-galactoseFood and Chemical Toxicology, 2009
- Differential regulation of BACE1 promoter activity by nuclear factor‐κB in neurons and glia upon exposure to β‐amyloid peptidesJournal of Neuroscience Research, 2007
- Neurodegenerative diseases and oxidative stressNature Reviews Drug Discovery, 2004
- Proteomic identification of oxidatively modified proteins in alzheimer’s disease brain. part I: creatine kinase BB, glutamine synthase, and ubiquitin carboxy-terminal hydrolase L-1Free Radical Biology & Medicine, 2002
- Oxidative Stress Increases Expression and Activity of BACE in NT2 NeuronsNeurobiology of Disease, 2002
- Expression of 8-oxoguanine DNA glycosylase is reduced and associated with neurofibrillary tangles in Alzheimer's disease brainActa Neuropathologica, 2001