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Journal Article

Citation

Endesfelder S, Zaak I, Weichelt U, Bührer C, Schmitz T. Free Radic. Biol. Med. 2014; 67: 221-234.

Affiliation

Department of Neonatology, Charité University Medical Center, Berlin, Germany. Electronic address: [email protected]

Copyright

(Copyright © 2013, Elsevier Publishing)

DOI

10.1016/j.freeradbiomed.2013.09.026

PMID

24129198

Abstract

Caffeine administered to preterm infants has been shown to reduce rates of cerebral palsy and cognitive delay, as compared to placebo. We investigated the neuroprotective potential of caffeine for the developing brain in a neonatal rat model featuring transient systemic hyperoxia. Using 6 day-old rat pups, we found that after 24h and 48h of 80% oxygen exposure, apoptotic (TUNEL+) cell numbers increased in the cortex, hippocampus, and central grey matter, but not in the hippocampus or DG. In the dentate gyrus, high oxygen exposure led to a decrease in the number of proliferating (Ki67+) cells and the number of Ki67+ cells double staining for nestin (immature neurons), doublecortin (progenitors), and NeuN (mature neurons). Absolute numbers of nestin+, doublecortin+, and NeuN+ cells also decreased after hyperoxia. This was mirrored in a decline of transcription factors expressed in immature neurons (Pax6, Sox2), progenitors (Tbr2), and mature neurons (Prox1, Tbr1). Administration of a single dose of caffeine (10mg/kg) prior to high oxygen exposure almost completely prevented these effects. Our findings suggest that caffeine exerts protection for neonatal neurons exposed to high oxygen, possibly via its antioxidant capacity.


Language: en

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