Repression of the Glucocorticoid Receptor Increases Hypoxic-Ischemic Brain Injury in the Male Neonatal Rat.

ABSTRACT: Hypoxic-ischemic encephalopathy (HIE) resulting from asphyxia is the most common cause of neonatal brain damage and results in significant neurological sequelae, including cerebral palsy. The current therapeutic interventions are extremely limited in improving neonatal outcomes. The present study tests the hypothesis that the suppression of endogenous glucocorticoid receptors (GRs) in the brain increases hypoxic-ischemic (HI) induced neonatal brain injury and worsens neurobehavioral outcomes through the promotion of increased inflammation. A mild HI treatment of P9 rat pups with ligation of the right common carotid artery followed by the treatment of 8% O₂ for 60 min produced more significant brain injury with larger infarct size in female than male pups. Intracerebroventricular

SUBMITTER: Knox-Concepcion KR 

PROVIDER: S-EPMC6678481 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature