A histopathological study of premature and mature infants with pontosubicular neuron necrosis: neuronal cell death in perinatal brain damage.

摘要: Perinatal hypoxic-ischemic brain damage is a major cause of neuronal and behavior deficits, in which the onset injury can be before, at or after birth, effects may delayed. Pontosubicular neuron necrosis (PSN) one perinatal its pathological peculiarity apoptosis. In this study, we investigated whether apoptotic cascade PSN used caspase-pathway not, hypoglycemia activated apoptosis not. Sections pons with without were stained using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) immunohistochemistry for glial fibrillary acidic protein (GFAP), Bcl-2, Bcl-x caspase 3. Additionally, performed immunoblot analysis TUNEL-positive cell was closely associated presence karyorrhexis. Under combination karyorrhectic cells, number cells premature brains significantly more than mature brains. Hypoxic-ischemic considered to easily lead infants. Moreover, as pathophysiology, activation contributed death from caspase-immunoexpression analyses. showed large higher expression The result severe background prematurity complicated by hypoxia and/or ischemia.