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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Effect of transient maternal hypotension on apoptotic cell death in foetal rat brain
Hamit Ozyürek1, Sibel Bayrak2, Bilge Pehlivanoğlu2
1Pediatric Neurology Unit, Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.
Background:
Intrauterine perfusion insufficiency induced by transient maternal hypotension has been reported to be associated with foetal brain malformations. However, the effects of maternal hypotension on apoptotic processes in the foetal brain have not been investigated experimentally during the intrauterine period.
Aims:
The aim of this study was to investigate the effects of transient maternal hypotension on apoptotic cell death in the intrauterine foetal brain.
Study Design:
Animal experimentation.
Methods:
Three-month-old female Wistar albino rats were allocated into four groups (n=5 each). The impact of hypoxic/ischemic injury induced by transient maternal hypotension on the 15th day of pregnancy (late gestation) in rats was investigated at 48 (H17 group) or 96 hours (H19 group) after the insult. Control groups underwent the same procedure except for induction of hypotension (C17 and H17 groups). Brain sections of one randomly selected foetus from each pregnant rat were histopathologically evaluated for hypoxic/ischemic injury in the metencephalon, diencephalon, and telencephalon by terminal transferase-mediated dUTP nick end labelling and active cysteine-dependent aspartate-directed protease-3 (caspase-3) positivity for cell death.
Results:
The number of terminal transferase-mediated dUTP nick end labelling (+) cells in all the areas examined was comparable in both hypotension and control groups. The H17 group had active caspase-3 (+) cells in the metencephalon and telencephalon, sparing diencephalon, whereas the C19 and H19 groups had active caspase-3 (+) cells in all three regions. The number of active caspase-3 (+) cells in the telencephalon in the H19 group was higher compared with the metencephalon and diencephalon and compared with H17 group (p<0.05).
Conclusion:
Our results suggest that prenatal hypoxic/ischemic injury triggers apoptotic mechanisms. Therefore, blockade of apoptotic pathways, considering the time pattern of the insult, may constitute a potential neuroprotective approach for the detrimental effects of prenatal hypoperfusion.
