Abstract | BACKGROUND: Perinatal hypoxia is a universal cause of death and neurological deficits in neonates worldwide. Activation of microglial NADPH oxidase 2 (NOX2) leads to oxidative stress and neuroinflammation, which may contribute to hypoxic damage in the developing brain. Dexmedetomidine has been reported to exert potent neuroprotection in several neurological diseases, but the mechanism remains unclear. We investigated whether dexmedetomidine acts through microglial NOX2 to reduce neonatal hypoxic brain damage. METHODS: The potential role of microglial NOX2 in dexmedetomidine-mediated alleviation of hypoxic damage was evaluated in cultured BV2 microglia and neonatal rats subjected to hypoxia. In vivo, neonatal rats received dexmedetomidine (25 μg/kg, i.p.) 30 min before or immediately after hypoxia (5% O2, 2 h). Apocynin-mediated NOX inhibition and lentivirus-mediated NOX2 overexpression were applied to further assess the involvement of microglial NOX2 activation. RESULTS: CONCLUSION:
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Authors | Xiaohui Chen, Dongtai Chen, Qiang Li, Shuyan Wu, Jiahao Pan, Yanling Liao, Xiaochun Zheng, Weian Zeng |
Journal | Oxidative medicine and cellular longevity
(Oxid Med Cell Longev)
Vol. 2021
Pg. 6643171
( 2021)
ISSN: 1942-0994 [Electronic] United States |
PMID | 33628369
(Publication Type: Journal Article)
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Copyright | Copyright © 2021 Xiaohui Chen et al. |
Chemical References |
- Acetophenones
- Cytokines
- Inflammation Mediators
- NF-kappa B
- Dexmedetomidine
- acetovanillone
- Cybb protein, rat
- NADPH Oxidase 2
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Topics |
- Acetophenones
(pharmacology)
- Animals
- Animals, Newborn
- Cells, Cultured
- Cognitive Dysfunction
(enzymology, etiology, pathology)
- Cytokines
(metabolism)
- Dexmedetomidine
(pharmacology)
- Enzyme Activation
(drug effects)
- Hippocampus
(pathology, ultrastructure)
- Hypoxia
(complications)
- Inflammation Mediators
(metabolism)
- Microglia
(drug effects, enzymology, pathology, ultrastructure)
- Models, Biological
- NADPH Oxidase 2
(antagonists & inhibitors, metabolism)
- NF-kappa B
(metabolism)
- Neuroprotection
(drug effects)
- Oxidative Stress
(drug effects)
- Rats, Sprague-Dawley
- Signal Transduction
(drug effects)
- Synapses
(drug effects, pathology, ultrastructure)
- Rats
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