ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024
Minocycline alleviates microglia ferroptosis by inhibiting HO-1 during cerebral ischemia-reperfusion injury.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed.
- In Vivo Longitudinal Mapping of Brain Iron Accumulation After Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2026Article
- No-reflow phenomenon after vessel recanalization in acute ischemic stroke: mechanisms, diagnosis, and treatment directions.Journal of neurology · 2026Review
- The Mechanism of Ferroptosis and Blood-Brain Barrier Damage in Cerebrovascular Diseases.Biomedicines · 2026Review
- MiR-122 activates PI3K/Akt signaling to suppress microglial activation and ferroptosis in ischemic brain injury.Metabolic brain disease · 2026Article
- Neuroinflammatory mechanisms and pharmacological advances in autism spectrum disorder: from inflammatory pathways to targeted interventions.Frontiers in immunology · 2026Review
- Stachyose supplementation attenuates ischemic stroke injury via gut-brain axis mediated adenine metabolism and neuroactive ligand-receptor signaling.Current research in food science · 2026Article
- Acupuncture in Cerebral Ischemia-Reperfusion Injury: A Mechanistic Narrative Review of Innate Immune Sensing and Regulated Cell Death-Related Inflammatory Amplification.International journal of general medicine · 2026Review
- Minocycline ameliorates CNS autoimmunity through restraint of CD4Frontiers in immunology · 2026Article
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Protective Effect of Chinese Herbal Medicine on Cerebral Ischemia-Reperfusion Injury by Regulating Ferroptosis.Drug design, development and therapy · 2026Review
- Ferroptosis in microglial activation: a systematic review and multidata comparison.Brain communications · 2026Review
- HIF-1α in ischemic stroke: context-dependent roles in ferroptosis and neurovascular repair.Frontiers in neurology · 2026Review
- Exploring the Nexus: How Ferroptosis, Microglia, and Neuroinflammation Converge in Ischemic Stroke Pathogenesis.Molecular neurobiology · 2025Review
- Oxidative cell death in the central nervous system: mechanisms and therapeutic strategies.Frontiers in cell and developmental biology · 2025Review
- Time and Tissue Windows in Futile Reperfusion after Ischemic Stroke.Aging and disease · 2024Article
- The interplay between ferroptosis and inflammation: therapeutic implications for cerebral ischemia-reperfusion.Frontiers in immunology · 2024Review
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9 authors.
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Abstract
objectiveIschemic stroke is a leading cause of death and disability in individuals worldwide. Cerebral ischemia-reperfusion injury (CIRI) typically results in severe secondary injury and complications following reperfusion therapy. Microglia play critical roles in the inflammatory reaction of CIRI. However, less attention has been given to microglial death in this process. Our study aims to explore microglial death in CIRI and the effects and mechanism of minocycline treatment on microglia.
methodsA middle cerebral artery occlusion (MCAO) model was applied to induce CIRI in rats. At 0 h, 24 h and 48 h post-operation, rats were intraperitoneally injected with 45 mg/kg minocycline. Neurological deficit scoring, 2,3,5-triphenyltetrazolium chloride (TTC) staining, assessment of activated microglia and examination of mitochondrial structure were conducted and checked at 72 h after reperfusion. Additionally, an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) model was established. BV-2 cells were treated with various pharmacological inhibitors of cell death or minocycline. Cell viability, lipid peroxidation, mitochondrial structure and function, and labile Fe
resultsIn the MCAO and OGD/R models, ferroptosis was identified as a major form of microglial death. Minocycline inhibited microglia ferroptosis by reducing HO-1 expression. In addition, minocycline improved mitochondrial membrane potential, mitochondrial structures and microglial survival in vivo. Minocycline also decreased labile Fe
conclusionFerroptosis is a major form of microglial death in CIRI. The protective mechanism of minocycline in CIRI partially hinges on its ability to effectively ameliorate microglia ferroptosis by downregulating HO-1 expression. Consequently, targeting microglia ferroptosis is a promising treatment for CIRI.
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