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Cited by 271Neuroinflammation and Neurodegeneration MechanismsAlcohol Consumption and Health EffectsTryptophan and brain disorders

Chronic ethanol treatment enhances inflammatory mediators and cell death in the brain and in astrocytes

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Vallés, Soraya L., Blanco, Ana M., Pascual, María, Guerri, Consuelo·2004·Brain Pathology
DOI 10.1111/j.1750-3639.2004.tb00079.xPMC PMC8095743
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Abstract

Inflammatory processes and cytokine expression have been implicated in the pathogenesis of several neurodegenerative disorders. Chronic ethanol intake induces brain damage, although the mechanisms involved in this effect are not well understood. We tested the hypothesis that activation of glial cells by ethanol would induce stimulation of signaling pathways and inflammatory mediators in brain, and would cause neurotoxicity. We used cerebral cortex from control and chronic ethanol-fed rats, which received ethanol-liquid diet for 5 months and cultured of astrocytes exposed to 75 mM ethanol for 7 days. Our results demonstrate that chronic ethanol treatment up-regulates iNOS, COX-2 and IL-1beta in rat cerebral cortex and in cultured astrocytes. Under both experimental conditions, up-regulation of these inflammatory mediators and IL-1RI concomitantly occurs with the stimulation of IRAK and MAP kinases, including ERK1/2, p-38 and JNK, which trigger the downstream activation of oxidant-sensitive transcription factors NF-KB and AP-1. These effects were associated with an increased in both caspase-3 and apoptosis in ethanol-fed rats and in astrocytes exposed to ethanol. In conclusion, chronic ethanol treatment stimulates glial cells, up-regulating the production and the expression of inflammatory mediators in the brain, and activating signalling pathways and transcription factors involved in inflammatory damage and cell death.

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Crossref · 10.1111/j.1750-3639.2004.tb00079.x

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  1. [52]52. Yamamoto Y, Gaynor RB (2004) IkappaB kinases: key regulators of the NF‐kappaB pathway. TRENDS Biochem Sci 29:72–79. [DOI] [PubMed] [Google Scholar] Articles from Brain Pathology are provided here courtesy of Wiley

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Authors
Vallés, S. L., Blanco, A. M., Pascual, M., & Guerri, C.
Corresponding author
Guerri, Consuelo
ORCID
Venue
Brain Pathology
Publisher
Wiley
Published
2004-10
Volume
14
Issue
4
Pages
365-371
ISSN
  • 1015-6305 (ISSN-L)
  • 1750-3639
DOI
10.1111/j.1750-3639.2004.tb00079.x
PMC
PMC8095743
OpenAlex
W2058339095
Cited by
271
References
52
Citations by year
2026: 2 · 2025: 12 · 2024: 10 · 2023: 11 · 2022: 15 · 2021: 12 · 2020: 21 · 2019: 14 · 2018: 13 · 2017: 20 · 2016: 17 · 2015: 18 · 2014: 19 · 2013: 19 · 2012: 20
FWCI
3.41
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 551 d)
Locations
  • Brain Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
chronic ethanol exposure, neuroinflammation, astrocytes, cerebral cortex, inducible nitric oxide synthase, cyclooxygenase-2, IL-1β, IL-1 receptor, IRAK, mitogen-activated protein kinase, ERK1/2, p38 MAPK, JNK, NF-κB, AP-1, caspase-3, apoptosis, neurotoxicity, glial activation
MeSH terms
Ethanol, Animals, Animals, Newborn, Astrocytes, Cells, Cultured, Central Nervous System Depressants, Cerebral Cortex, Enzyme-Linked Immunosorbent Assay, Female, Gene Expression Regulation, Interleukin-1, Isoenzymes, Prostaglandin-Endoperoxide Synthases, RNA, Messenger, Blotting, Western, Cell Death, Rats, Wistar, Transcription Factor AP-1, Nitric Oxide Synthase, Reverse Transcriptase Polymerase Chain Reaction, Caspases, I-kappa B Proteins, Mitogen-Activated Protein Kinase Kinases, Electrophoretic Mobility Shift Assay, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 3, MAP Kinase Kinase 4, Rats, Cyclooxygenase 2, Nitric Oxide Synthase Type II, Caspase 3, DNA Fragmentation

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