ArticleNeural regeneration research2013
Inhibition of inflammatory mediator release from microglia can treat ischemic/hypoxic brain injury.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Purinergic signaling: a potential therapeutic target for depression and chronic pain.Purinergic signalling · 2023Review
- Adrenomedullin: an important participant in neurological diseases.Neural regeneration research · 2020Review
- Metabolic Reprograming of Microglia in the Regulation of the Innate Inflammatory Response.Frontiers in immunology · 2020Review
- Fas-ligand and interleukin-6 in the cerebrospinal fluid are early predictors of hypoxic-ischemic encephalopathy and long-term outcomes after birth asphyxia in term infants.Journal of neuroinflammation · 2018Article
- Article
- Mst1: Function and Mechanism in Brain and Myocardial Ischemia Reperfusion Injury.Current neuropharmacology · 2018Review
- Neuroprotective Effect of Paroxetine on Memory Deficit Induced by Cerebral Ischemia after Transient Bilateral Occlusion of Common Carotid Arteries in Rat.Iranian journal of pharmaceutical research : IJPR · 2018Article
- Combined effects of age and polymorphisms in Notch3 in the pathogenesis of cerebral infarction disease.Metabolic brain disease · 2016Article
- Correlating interleukin-10 promoter gene polymorphisms with human cerebral infarction onset.Neural regeneration research · 2015Article
- Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage.Neural regeneration research · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inflammatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β.
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