Minocycline protects developing brain against ethanol-induced damage.

Szczegóły
Abstrakt

Tytuł:: Minocycline protects developing brain against ethanol-induced damage.
Autorzy:: Wang X; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Zhang K; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Yang F; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Ren Z; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA; Department of Anatomy, School of Basic Medicine, Anhui Medical University, Hefei, Anhui 230032, China.
Xu M; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Frank JA; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Ke ZJ; Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Luo J; Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA; Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address: .
Źródło:: Neuropharmacology [Neuropharmacology] 2018 Feb; Vol. 129, pp. 84-99. Date of Electronic Publication: 2017 Nov 14.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Publication: Oxford : Pergamon Press
Original Publication: Oxford, New York, Pergamon.
MeSH Terms:: Brain*/drug effects
Brain*/growth & development
Brain*/metabolism
Brain Injuries/*drug therapy
Cytokines/*metabolism
Encephalitis/*drug therapy
Minocycline/*therapeutic use
Neuroprotective Agents/*therapeutic use
Animals ; Animals, Newborn ; Brain Injuries/chemically induced ; CREB-Binding Protein/genetics ; CREB-Binding Protein/metabolism ; Calcium-Binding Proteins/metabolism ; Caspase 3/metabolism ; Cells, Cultured ; Central Nervous System Depressants/toxicity ; Cerebral Cortex/cytology ; Cytokines/genetics ; Enzyme Inhibitors/therapeutic use ; Ethanol/toxicity ; Glycogen Synthase Kinase 3 beta/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/metabolism ; Microglia/drug effects ; Neurons/drug effects ; Signal Transduction/drug effects
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Grant Information:: I01 BX001721 United States BX BLRD VA; R01 AA015407 United States AA NIAAA NIH HHS; R01 AA017226 United States AA NIAAA NIH HHS
Contributed Indexing:: Keywords: Apoptosis; Development; Fetal alcohol syndrome; Inflammation; Microglia; Neurodegeneration
Substance Nomenclature:: 0 (Aif1 protein, mouse)
0 (Calcium-Binding Proteins)
0 (Central Nervous System Depressants)
0 (Cytokines)
0 (Enzyme Inhibitors)
0 (Microfilament Proteins)
0 (Neuroprotective Agents)
3K9958V90M (Ethanol)
EC 2.3.1.48 (CREB-Binding Protein)
EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
EC 2.7.11.1 (Gsk3b protein, mouse)
EC 3.4.22.- (Caspase 3)
FYY3R43WGO (Minocycline)
Entry Date(s):: Date Created: 20171118 Date Completed: 20180727 Latest Revision: 20190201
Update Code:: 20240105
PubMed Central ID:: PMC5714686
DOI:: 10.1016/j.neuropharm.2017.11.019
PMID:: 29146504
: Czasopismo naukowe

Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during the pregnancy and is the leading cause of mental retardation. Ethanol exposure during the development results in the loss of neurons in the developing brain, which may underlie many neurobehavioral deficits associated with FASD. It is important to understand the mechanisms underlying ethanol-induced neuronal loss and develop appropriate therapeutic strategies. One of the potential mechanisms involves neuroimmune activation. Using a third trimester equivalent mouse model of ethanol exposure, we demonstrated that ethanol induced a wide-spread neuroapoptosis, microglial activation, and neuroinflammation in C57BL/6 mice. Minocycline is an antibiotic that inhibits microglial activation and alleviates neuroinflammation. We tested the hypothesis that minocycline may protect neurons ethanol-induced neuron death by inhibiting microglial activation and neuroinflammation. We showed that minocycline significantly inhibited ethanol-induced caspase-3 activation, microglial activation, and the expression of pro-inflammatory cytokines. In contrast, minocycline reversed ethanol inhibition of anti-inflammatory cytokines. Minocycline blocked ethanol-induced activation of GSK3β, a key mediator of neuroinflammation and microglial activation in the developing brain. Consistent with the in vivo observations, minocycline inhibited ethanol-induced the expression of pro-inflammatory cytokines and activation of GSK3β in a microglia cell line (SIM-9). GSK3β inhibitor eliminated ethanol activation of pro-inflammatory cytokines in SIM-9 cells. Co-cultures of cortical neurons and SIM-9 microglia cells sensitized neurons to alcohol-induced neuronal death. Minocycline protected neurons against ethanol-induced neuronal death in neurons/microglia co-cultures. Together, these results suggest that minocycline may ameliorate ethanol neurotoxicity in the developing by alleviating GSK3β-mediated neuroinflammation.
(Copyright © 2017 Elsevier Ltd. All rights reserved.)

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