Journal
DEVELOPMENTAL NEUROSCIENCE
Volume 31, Issue 5, Pages 420-426Publisher
KARGER
DOI: 10.1159/000232560
Keywords
Mixed lineage kinase inhibition; Neonatal hypoxia-ischemia; Brain injury; Apoptosis; Inflammation
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Funding
- MRC [G0802853] Funding Source: UKRI
- Medical Research Council [G0802853, P19381] Funding Source: Medline
- Medical Research Council [G0802853] Funding Source: researchfish
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Hypoxic-ischemic brain injury is often delayed and involves both apoptotic and immunoregulatory mechanisms. In this study, we used a neonatal model of hypoxia-ischemia to examine the effect of the mixed lineage kinase (MLK) inhibitor CEP-1347 on brain damage, apoptosis and inflammation. The tissue volume loss was reduced by 28% (p = 0.019) in CEP-1347-treated versus vehicle-treated rats and CEP-1347 significantly attenuated microgliosis at 7 days (p = 0.038). CEP-1347 decreased TUNEL-positive staining as well as cleaved caspase 3 immunoreactivity. CEP-1347 did not affect the expression of pro-inflammatory cytokines IL-1 beta, IL-6 and MCP-1, nor did it affect the expression of OX-42 (CR3) and OX-18 (MHC I) 24 h after the insult. In conclusion, the MLK inhibitor CEP-1347 has protective effects in a neonatal rat model of hypoxia-ischemia, which is mainly related to reduced apoptosis. Copyright (C) 2009 S. Karger AG, Basel
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