Introduction The birth of most mammals features a dramatic increase in oxygen
while placenta-derived hormones such as β-estradiol and progesterone plummet.
In experimental newborn animals, transiently elevated oxygen concentrations
cause death of neurons, astrocytes, and oligodendrocyte precursors. High
oxygen has been associated with cerebral palsy in human preterm infants while
progesterone is being used to prevent preterm delivery and investigated as a
neuroprotective agent. Methods In this study, we investigated the effects of
hyperoxia (80% O2 for 24, 48, and 72 h) on cultured C8-D1A astrocytes in the
presence or absence of progesterone at concentrations ranging from 10−9 to
10−5 mol/L. Results Hyperoxia measured by methytetrazolium assay (MTT) reduced
cell viability, increased release of lactate dehydrogenase (LDH), reduced
carboxyfluorescein diacetate succinimidyl ester (CFSE)-assessed cell
proliferation, and downregulated Cylin D2 expression. Progesterone did not
affect any of these hyperoxia-mediated indicators of cell death or
malfunctioning. Real-time PCR analysis showed that hyperoxia caused
downregulation of the progesterone receptors PR-AB und PR-B. Conclusions Our
experiments showed that there was no protective effect of progesterone on
hyperoxia-inducted cell damage on mouse C8-D1A astrocytes. Down regulation of
the progesterone receptors might be linked to the lack of protective effects
