Cited by 112Neonatal and fetal brain pathologyNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular Disturbances

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Brain Injury Induced by Intracerebral Injection of Interleukin-1beta and Tumor Necrosis Factor-alpha in the Neonatal Rat

Cai, Zhengwei, Lin, Shuying, Pang, Yi, Rhodes, Philip G·2004·Pediatric Research

DOI 10.1203/01.pdr.0000134249.92944.14

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Abstract

To examine the possible role of inflammatory cytokines in mediating neonatal brain injury, we investigated effects of intracerebral injection of IL-1beta (IL-1beta) or tumor necrosis factor-alpha (TNFalpha) on brain injury in the neonatal rat. A stereotaxic intracerebral injection of IL-1beta or TNFalpha (10 ng per pup) was performed in postnatal day 5 (P5) SD rats. Although no necrosis of neurons was found, increased astrogliosis, as indicated by GFAP positive staining was observed 24 and 72 h following the injection of IL-1beta or TNFalpha. IL-1beta induced apoptotic cell death in the rat brain 24 h after the injection, as indicated by increases in positive TUNEL staining and caspase-3 activity, and apoptotic cell death was partially blocked by systemic administration of NBQX, an antagonist of the AMPA glutamate receptor. IL-1beta also significantly reduced the number of developing oligodendrocytes (OLs) 24 h after the injection and this impairment was not prevented by NBQX. On the contrary, TNFalpha induced a much smaller increase in the number of TUNEL positive cells and did not reduce the number of developing OLs. By P8, myelin basic protein (MBP) was clearly detected in the control rat brain, while MBP positive staining was very weak, if any, in the IL-1beta treated rat brain. MBP expression in the TNFalpha treated rat brain was less affected. The overall results indicate that IL-1beta may directly cause injuries to developing OLs and impair myelination in the neonatal rat brain and TNFalpha may have different roles in mediating brain injury.

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Authors: Cai, Z., Lin, S., Pang, Y., & Rhodes, P. G.
Affiliations: University of Mississippi Medical Center (US)
Corresponding author: Cai, Zhengwei
ORCID: Cai, Zhengwei
Pang, Yi
Venue: Pediatric Research
Publisher: Springer Science and Business Media LLC
Published: 2004-09
Volume: 56
Issue: 3
Pages: 377-384
ISSN: 0031-3998 (ISSN-L)
1530-0447
DOI: 10.1203/01.pdr.0000134249.92944.14
OpenAlex: W2004941059
Cited by: 111
References: 46
Citations by year: 2026: 4 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 7 · 2021: 4 · 2020: 9 · 2019: 8 · 2018: 6 · 2017: 7 · 2016: 4 · 2015: 3 · 2014: 3 · 2013: 6 · 2012: 7
FWCI: 2.65
Type: journal article
Language: en
Open access: closed
Locations: Pediatric Research (publishedVersion)
PubMed (publishedVersion)
Funders: Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD35496)
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 › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords: neonatal brain injury, IL-1β, TNF-α, inflammatory cytokines, astrocyte activation, glial fibrillary acidic protein, neuronal apoptosis, caspase-3, NBQX, oligodendrocyte development, myelination, myelin basic protein, intracerebral injection, postnatal rat brain
MeSH terms: Animals, Animals, Newborn, Brain Injuries, Cerebral Cortex, Myelin Basic Protein, Humans, Infant, Inflammation, Interleukin-1, Oligodendroglia, Quinoxalines, Tumor Necrosis Factor-alpha, Rats, Sprague-Dawley, Apoptosis, Receptors, AMPA, Excitatory Amino Acid Antagonists, Caspases, In Situ Nick-End Labeling, Rats, Caspase 3

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Brain Injury Induced by Intracerebral Injection of Interleukin-1beta and Tumor Necrosis Factor-alpha in the Neonatal Rat

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