Article

Interleukin-1beta-induced brain injury in the neonatal rat can be ameliorated by alpha-phenyl-n-tert-butyl-nitrone.

Department of Pediatrics, Division of Newborn Medicine, University of Mississippi Medical Center, Jackson, MS 39216-4504, USA.
Experimental Neurology (impact factor: 4.7). 09/2009; 220(1):143-53. DOI:10.1016/j.expneurol.2009.08.003 pp.143-53
Source: PubMed

ABSTRACT 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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Keywords

1 microg/kg
 
acute brain injury
 
attenuated oxidative stress induced
 
beta-amyloid precursor protein
 
brain injury
 
IL-1beta exposure
 
IL-1beta induced perinatal brain injury
 
IL-1beta injection
 
inflammatory cytokines
 
Intracerebral administration
 
intracerebral injection
 
lipopolysaccharide
 
mediating brain injury
 
mediating perinatal brain injury
 
neonatal rat
 
neonatal rat brain
 
oligodendrocytes
 
tyrosine hydroxylase-positive neurons
 
ventral tegmental areas
 
ventricles bilaterally
 

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