cytochrome-c-t and Bronchopulmonary-Dysplasia

Neonatal bronchopulmonary dysplasia (BPD) might lead to an increased risk for brain injury. The present study aims to investigate the effects of neonatal BPD on neuronal apoptosis in the hippocampus and cognitive function and to explore the underlying mechanisms. The results revealed that BPD model rat pups exhibited more apoptotic cells in the hippocampus and longer escape latencies in the Morris maze test. Both the caspase-dependent and caspase-nondependent signal pathways were activated. Further examinations showed an elevated p53 level by BPD via HIF-1α induction, while the caspase-3 in the hippocampus was suppressed by both HIF-1α and p53 inhibitor. These findings suggested that neonatal BPD caused impaired cognitive function and neuron apoptosis in hippocampus via p53 and HIF-1α. Although the precise mechanism requires further investigation, this study provided new evidence for and an explanation of the impaired CNS developmental outcomes of BPD.

Topics: Animals; Animals, Newborn; Apoptosis; bcl-2-Associated X Protein; Bronchopulmonary Dysplasia; Caspase 3; Caspase 8; Caspase 9; Collagen; Cytochromes c; Disease Models, Animal; fas Receptor; Hippocampus; Hypoxia-Inducible Factor 1, alpha Subunit; Lung; Maze Learning; Mitochondria; Neurons; Rats, Sprague-Dawley; Tumor Suppressor Protein p53