ArticleThe Journal of thoracic and cardiovascular surgery2018
Inhibition of microglial activation by minocycline reduced preoligodendrocyte injury in a neonatal rat brain slice model.
Article in The Journal of thoracic and cardiovascular surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 16 citations in OpenAlex.
- Microglia Pyroptosis-Derived IL-18 Drives White Matter Injury in Developing Brain following Hypothermic Hypoxia-Ischemia.Neuroscience bulletin · 2026Article
- Gut microbiota-derived cholic acid mediates neonatal brain immaturity and white matter injury under chronic hypoxia.iScience · 2024Article
- Microglial diversity along the hippocampal longitudinal axis impacts synaptic plasticity in adult male mice under homeostatic conditions.Journal of neuroinflammation · 2022Article
- Triptolide protects against white matter injury induced by chronic cerebral hypoperfusion in mice.Acta pharmacologica Sinica · 2022Article
- Minocycline attenuation of rat corpus callosum abnormality mediated by low-dose lipopolysaccharide-induced microglia activation.Journal of neuroinflammation · 2021Article
- Application of a neuroscience research model to study neuroprotection in children with congenital heart disease.The Journal of thoracic and cardiovascular surgery · 2018Article
- Generation of an Iba1-EGFP Transgenic Rat for the Study of Microglia in an Outbred Rodent Strain.eNeuroArticle
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10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundPeriventricular leukomalacia is a common white-matter injury after neonatal cardiac surgery; however, its potential cellular mechanism remains uncertain. There is limited study regarding periventricular leukomalacia treatment.
methodsA neonatal rat brain slice perfusion model was used for reproducing the condition of cardiopulmonary bypass, and oxygen glucose deprivation simulated circulatory arrest. Seven-day-old Sprague-Dawley rats were randomly divided into 7 groups: (1) control group with 36°C; (2) 60 minutes of oxygen glucose deprivation group on 15°C, 25°C, 36°C, respectively; and (3) 60 minutes of oxygen glucose deprivation group on 15°C, 25°C, 36°C, plus minocycline (10 μmol/L), respectively. Immunohistochemistry, Western blot, and inflammatory mediators were compared after the perfusion procedures in the different groups.
resultsThis neonatal rat brain slice perfusion with oxygen glucose deprivation model could replicate the pathophysiologic process and injury after cardiopulmonary bypass and hypothermic circulatory arrest. With the increase of oxygen glucose deprivation perfusion temperature, we found that both microglia activation and preoligodendrocyte loss increased. The application of minocycline can significantly inhibit microglial activation and preoligodendrocyte cells loss in the normothermic (36°C) and moderate hypothermia (25°C) oxygen glucose deprivation groups (P < .05), with accompanying significant decreasing microglial inflammatory productions; however, no significant improvement was found in the deep hypothermia (15°C) group.
conclusionsThe microglial activation may play a key role in preoligodendrocyte injury in the ex vivo neonatal rat brain slice perfusion and circulatory arrest model. Inhibition of microglial activation with minocycline may be an attractive target for white-matter protection during cardiopulmonary bypass and hypothermic circulatory arrest.
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