Interleukin-1β-induced brain injury in the neonatal rat can be ameliorated by α-phenyl-n-tert-butyl-nitrone
Open accessAbstract
To examine the possible role of inflammatory cytokines in mediating perinatal brain injury, we investigated effects of intracerebral injection of interleukin-1beta (IL-1beta) on brain injury in the neonatal rat and the mechanisms involved. Intracerebral administration of IL-1beta (1 microg/kg) resulted in acute brain injury, as indicated by enlargement of ventricles bilaterally, apoptotic death of oligodendrocytes (OLs) and loss of OL immunoreactivity in the neonatal rat brain. IL-1beta also induced axonal and neuronal injury in the cerebral cortex as indicated by elevated expression of beta-amyloid precursor protein, short beaded axons and dendrites, and loss of tyrosine hydroxylase-positive neurons in the substantia nigra and the ventral tegmental areas. Administration of alpha-phenyl-n-tert-butyl-nitrone (PBN, 100 mg/kg i.p.) immediately after the IL-1beta injection protected the brain from IL-1beta-induced injury. Protection of PBN was linked with the attenuated oxidative stress induced by IL-1beta, as indicated by decreased elevation of 8-isoprostane content and by the reduced number of 4-hydroxynonenal or malondialdehyde or nitrotyrosine-positive cells following IL-1beta exposure. PBN also attenuated IL-1beta-stimulated inflammatory responses as indicated by the reduced activation of microglia. The finding that IL-1beta induced perinatal brain injury was very similar to that induced by lipopolysaccharide (LPS), as we previously reported and that PBN was capable to attenuate the injury induced by either LPS or IL-1beta suggests that IL-1beta may play a critical role in mediating brain injury associated with perinatal infection/inflammation.
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Neonatal administration of inflammatory cytokines such as Il-1β reduces the number of developing oligodendrocytes.
“Neonatal administration of inflammatory cytokines such as Il-1β reduces the number of developing oligodendrocytes (Cai et al., 2004; Fan et al., 2009).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Fan et al., 2009
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- Authors
- Fan, L.-W., Mitchell, H. J., Tien, L.-T., Rhodes, P. G., & Cai, Z.
- Affiliations
- University of Mississippi Medical Center (US)
- Fu Jen Catholic University (TW)
- Corresponding author
- Cai, Zhengwei
- ORCID
- Cai, Zhengwei
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 220
- Issue
- 1
- Pages
- 143-153
- ISSN
- 0014-4886 (ISSN-L)
- PMC
- PMC2761495
- OpenAlex
- W2005855352
- Cited by
- 26
- References
- 57
- Citations by year
- 2023: 1 · 2022: 1 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 1
- FWCI
- 2.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS054278, R56NS054278, NS54278)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD35496, R29HD035496, R01HD035496)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- IL-1β, perinatal brain injury, N-tert-butyl-alpha-phenylnitrone, neuroprotection, oxidative stress, microglial activation, oligodendrocyte apoptosis, substantia nigra neurons, ventral tegmental area, lipopolysaccharide, perinatal infection, inflammatory cytokines, 8-isoprostane, nitrotyrosine, malondialdehyde
- MeSH terms
- Animals, Animals, Newborn, Brain, Brain Damage, Chronic, Cyclic N-Oxides, Disease Models, Animal, Encephalitis, Female, Gliosis, Lipopolysaccharides, Male, Nerve Degeneration, Oligodendroglia, Cell Death, Microglia, Oxidative Stress, Neuroprotective Agents, Inflammation Mediators, Cytoprotection, Rats, Interleukin-1beta
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