Protection of the Developing Brain with Anthocyanins Against Ethanol-Induced Oxidative Stress and Neurodegeneration
- Authors
- Shah, Shahid Ali; Yoon, Gwang Ho; Kim, Myeong Ok
- Issue Date
- Jun-2015
- Publisher
- SPRINGER
- Keywords
- Apoptosis; Hippocampus; Intracellular signaling; NF-kappa B; COX-2
- Citation
- MOLECULAR NEUROBIOLOGY, v.51, no.3, pp.1278 - 1291
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULAR NEUROBIOLOGY
- Volume
- 51
- Number
- 3
- Start Page
- 1278
- End Page
- 1291
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/17239
- DOI
- 10.1007/s12035-014-8805-7
- ISSN
- 0893-7648
- Abstract
- Oxidative stress has been implicated in the pathophysiology of several neurodegenerative disorders. Numerous studies have reported that ethanol exposure produces reactive oxygen species (ROS), one of the best-known molecular mechanisms of ethanol neurotoxicity. We recently reported gamma-aminobutyric acid B1 receptor (GABA(B1)R)-dependent protection by anthocyanins against ethanol-induced apoptosis in prenatal hippocampal neurons. Here, we examined the effect of anthocyanin neuroprotection against ethanol in the hippocampus of the postnatal day-7 rat brain. After 4 h of ethanol administration, either alone or together with anthocyanin, the expression of glutamate receptors (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs)), intracellular signaling molecules, and various synaptic, inflammatory, and apoptotic markers was evaluated. The results suggest that anthocyanins significantly reversed the ethanol-induced inhibition of glutamatergic neurotransmission, synaptic dysfunction, GABA(B1)R activation, and neuronal apoptosis by stimulating the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/v-akt murine thymoma viral oncogene (Akt)/glycogen synthase kinase 3 beta (GSK3 beta) pathway in the hippocampus of postnatal rat brain. Anthocyanins also inhibited the ethanol-activated expression of phosphorylated c-Jun N terminal kinase (p-JNK), phospho-nuclear factor kappa B (p-NF-kappa B), cyclooxygenase 2 (COX-2), as well as attenuating neuronal apoptosis in the hippocampal CA1, CA3 and DG regions of the developing rat brain. Furthermore, anthocyanins increased cell viability, attenuated ethanol-induced PI3K-dependent ROS production, cytotoxicity, and caspase-3/7 activation in vitro. In conclusion, these results suggest that anthocyanins are beneficial against ethanol abuse during brain development.
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