Abstract
Background and aims: Erythropoietin is a known neuroprotective agent in the presence of EpoR and CD131. Hypoxia may induce EpoR and increase rhEPO binding in peripheral tissue. We wanted to study whether rhEPO is protective in mice preconditioned with hypoxemia in a cyanosis model.
Methods: 50 neonatal transgenic cerebral luciferase-NFκB reporter mice from 7 litters were used. At the day of birth 3 litters and mothers were kept in a hypoxic environment (FiO2=0.12), while 4 litters were kept under normoxic conditions. At day seven, five hypoxemic mice and 14 normoxemic mice pre-treated with rhEPO, underwent selective occlusion of the left carotic artery and hypoxia (4% oxygen) together with 15 hypoxemic and 15 normoxemic mice. Signals were measured from the ex vivo left hemisphere as luminescence (log-transformed), and compared to normoxemia + rhEPO mice that were expected to have the least neuronal damage. Weight was used as a covariate. Values are estimated means ± SEM based on weight 3.77g.
Results: Normoxemia + rhEPO and hypoxemia was not different (7.61±0.04 vs. 7.67±0.04), while normoxia alone, and hypoxemia + rhEPO had significantly higher expression of NFκB than normoxemia + rhEPO (7.91±0.04; 7.88±0.06 vs. 7.61±0.04, p< 0.05).
Conclusion: Erythropoietin increases NFκB expression in hypoxemic preconditioned mice comparable to the increase of NFκB in not treated normoxemic mice after cerebral insult. This indicates that rhEPO may be detrimental in hypoxemic mice and warrants further studies before using rhEPO as a presumptive neuroprotective agent in cyanotic individuals.
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Odland, H., Aasland, A., Carlsen, H. et al. 247 Neuroprotection with Rhepo in Cyantoic Neonatal Mice. Pediatr Res 68 (Suppl 1), 128 (2010). https://doi.org/10.1203/00006450-201011001-00247
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DOI: https://doi.org/10.1203/00006450-201011001-00247