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Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression

1
Department of Anatomy, Dongguk University College of Medicine, Gyeongju 38066, Korea
2
Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University, Mymensingh-2202, Bangladesh
3
Department of Fisheries Biology and Genetics, Patuakhali Science and Technology University, Patuakhali-8602, Bangladesh
4
Department of Fishing and Post Harvest Technology, Sher-e-Bangla Agricultural University, Sher-e-Bangla Nagar, Dhaka-1207, Bangladesh
5
Department of Biotechnology, Pukyong National University, Namku, Busan 608-737, Korea
*
Author to whom correspondence should be addressed.
Antioxidants 2020, 9(3), 223; https://doi.org/10.3390/antiox9030223
Received: 31 December 2019 / Revised: 4 March 2020 / Accepted: 6 March 2020 / Published: 9 March 2020
(This article belongs to the Special Issue Hypoxia-Induced Oxidative Stress in the Brain)
Oxidative stress is known to be critically implicated in the pathophysiology of several neurological disorders, including Alzheimer’s disease and ischemic stroke. The remarkable neurotrophic activity of Gelidium amansii, which has been reported consistently in a series of our previous studies, inspired us to investigate whether this popular agarophyte could protect against hypoxia/reoxygenation (H/R)-induced oxidative injury in hippocampal neurons. The primary culture of hippocampal neurons challenged with H/R suffered from a significant loss of cell survival, accompanied by apoptosis and necrosis, DNA damage, generation of reactive oxygen species (ROS), and dissipation of mitochondrial membrane potential (ΔΨm), which were successfully attenuated when the neuronal cultures were preconditioned with ethanolic extract of G. amansii (GAE). GAE also attenuated an H/R-mediated increase of BAX and caspase 3 expressions while promoting Bcl-2 expression. Moreover, the expression of N-methyl-d-acetate receptor subunit 2B (GluN2B), an extrasynaptic glutamate receptor, was significantly repressed, while synaptic GluN2A expression was preserved in GAE-treated neurons as compared to those without GAE intervention. Together, this study demonstrates that GAE attenuated H/R-induced oxidative injury in hippocampal neurons through, at least in part, a potential neuroprotective mechanism that involves inhibition of GluN2B-mediated excitotoxicity and suppression of ROS production, and suggests that this edible seaweed could be a potential source of bioactive metabolites with therapeutic significance against oxidative stress-related neurodegeneration, including ischemic stroke and neurodegenerative diseases. View Full-Text
Keywords: oxidative stress; reactive oxygen species; hypoxia-reoxygenation; GluN2B; CNS neuron; Gelidium amansii oxidative stress; reactive oxygen species; hypoxia-reoxygenation; GluN2B; CNS neuron; Gelidium amansii
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MDPI and ACS Style

Hannan, M.A.; Haque, M.N.; Mohibbullah, M.; Dash, R.; Hong, Y.-K.; Moon, I.S. Gelidium amansii Attenuates Hypoxia/Reoxygenation-Induced Oxidative Injury in Primary Hippocampal Neurons through Suppressing GluN2B Expression. Antioxidants 2020, 9, 223.

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