ArticleInternational journal of biological sciences2025
Melatonin Ameliorate neuroinflammation in activated microglia through the Aryl hydrocarbon-Nrf2 axis.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- Validation of Paw Skin Hyperspectral Imaging for Assessing Neuropathic Pain Severity in a Chronic Constriction Injury Model.International journal of molecular sciences · 2026Article
- Integrative Multi-Omics Analysis Reveals the Immunoregulatory Effects of Sepia Ink on ADHD-like Phenotypes.Current issues in molecular biology · 2026Article
- The Metabolic Calibration of Female Immune Plasticity: From X-Linked Vulnerability to Precision Metabotyping.Biology · 2026Review
- Indole compounds produced by gut microbiota after metabolizing tryptophan improve dysmotility in sepsis via the AHR-TRPA1 axis in enteric nerves.BMC microbiology · 2025Article
- ROS homeostasis in cell fate, pathophysiology, and therapeutic interventions.Molecular biomedicine · 2025Review
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Authors and funding
10 authors.
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Abstract
Microglia-mediated neuroinflammation is central to many neurological disorders. The Aryl hydrocarbon receptor (AhR) is highly expressed in microglia and plays a key role in neuroinflammation. While melatonin has anti-inflammatory effects in neurodegenerative disorders, its connection to AhR in modulating neuroinflammation is unclear. This study found that melatonin inhibits NF-κB activity, reduces pro-inflammatory mediators, and promotes an M2 microglia profile. Melatonin also enhances phospho-AhR (Tyr239) activation, increases Nrf2 expression, and decreases LPS-induced ROS generation in microglia. Melatonin's effects are similar to those achieved by AhR activation. In contrast, AhR knockout worsens neurological deficits and microglial activation, while melatonin reverses these effects by restoring AhR expression. In conclusion, effects of melatonin on microglia-mediated neuroinflammation are closely linked to phospho-AhR (Tyr239) activation and its associated downstream gene, Nrf2, via the AhR/Nrf2/ARE pathway. Therefore, melatonin, in conjunction with AhR may offer promising therapeutic benefits in neuroinflammatory disorders.
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