ArticleGlia2015
Interleukin-1β protects astrocytes against oxidant-induced injury via an NF-κB-dependent upregulation of glutathione synthesis.
Article in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- Arsenite-Mediated Transcriptional Regulation of Glutathione Synthesis in Mammalian Primary Cortical Astrocytes.International journal of molecular sciences · 2025Article
- Neuroimmune regulation of the prefrontal cortex tetrapartite synapse.Neuropharmacology · 2025Review
- Nrf2 Regulates Basal Glutathione Production in Astrocytes.International journal of molecular sciences · 2025Article
- Effects of Diclofenac Sodium on Seizure Activity in Rats with Pentylenetetrazole-Induced Convulsions.Neurochemical research · 2023Article
- Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies.Frontiers in immunology · 2022Review
- Novel therapeutic modulators of astrocytes for hydrocephalus.Frontiers in molecular neuroscience · 2022Review
- Cystine-glutamate antiporter deletion accelerates motor recovery and improves histological outcomes following spinal cord injury in mice.Scientific reports · 2021Article
- Effects of Diclofenac Versus Meloxicam in Pentylenetetrazol-Kindled Mice.Neurochemical research · 2020Article
- Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression.Molecular biology reports · 2020Review
- The role of astrocytes in oxidative stress of central nervous system: A mixed blessing.Cell proliferation · 2020Review
- Riluzole: a therapeutic strategy in Alzheimer's disease by targeting the WNT/β-catenin pathway.Aging · 2020Article
- Genetic targeting of astrocytes to combat neurodegenerative disease.Neural regeneration research · 2020Article
- Nuclear Factor κB (NF-κB)-Mediated Inflammation in Multiple Sclerosis.Frontiers in immunology · 2020Review
- Reductive Reprogramming: A Not-So-Radical Hypothesis of Neurodegeneration Linking Redox Perturbations to Neuroinflammation and Excitotoxicity.Cellular and molecular neurobiology · 2019Review
- Astrocyte Antioxidant Systems.Antioxidants (Basel, Switzerland) · 2018Article
- Interleukin-1β Protects Neurons against Oxidant-Induced Injury via the Promotion of Astrocyte Glutathione Production.Antioxidants (Basel, Switzerland) · 2018Article
- Transport of BMAA into Neurons and Astrocytes by System xNeurotoxicity research · 2018Article
- Loss of NLRX1 Exacerbates Neural Tissue Damage and NF-κB Signaling following Brain Injury.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Cysteine, Glutathione, and Thiol Redox Balance in Astrocytes.Antioxidants (Basel, Switzerland) · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Astrocytes produce and export the antioxidant glutathione (GSH). Previously, we found that interleukin-1β (IL-1β) enhanced the expression of astrocyte system xc (-) , the transporter that delivers the rate-limiting substrate for GSH synthesis-cyst(e)ine. Herein, we demonstrate directly that IL-1β mediates a time-dependent increase in extracellular GSH levels in cortical astrocyte cultures, suggesting both enhanced synthesis and export. This increased GSH production was blocked by inhibition of nuclear factor-κB (NF-κB) activity but not by inhibition of p38 MAPK. To determine whether this increase could provide protection against oxidative stress, the oxidants tert-butyl hydroperoxide (tBOOH) and ferrous sulfate (FeSO4 ) were employed. IL-1β treatment prevented the increase in reactive oxygen species produced in astrocytes following tBOOH exposure. Additionally, the toxicity induced by tBOOH or FeSO4 exposure was significantly attenuated following treatment with IL-1β, an effect reversed by concomitant exposure to l-buthionine-S,R-sulfoximine (BSO), which prevented the IL-1β-mediated rise in GSH production. IL-1β failed to increase GSH or to provide protection against t-BOOH toxicity in astrocyte cultures derived from IL-1R1 null mutant mice. Overall, our data indicate that under certain conditions IL-1β may be an important stimulus for increasing astrocyte GSH production, and potentially, total antioxidant capacity in brain, via an NF-κB-dependent process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.