Cyclooxygenase-2 (COX-2) is known to be expressed in rat brain and up-regulated by ischemia. The administration of COX inhibitors before as well as soon after the ischemic insult reduces the extension of cerebral damage in rats. Overexpression of COX-2 has also been shown in the ischemic brain of adult human patients, while no information concerning COX-2 expression in neonatal ischemia is available. Intrapartum asphyxia and perinatal brain injury may result in cerebral palsy, mental retardation or epilepsy. COX-2 expression in the brain of neonates delivered after severe birth asphyxia was investigated using immunohistochemistry. Meningeal vessel walls of term and preterm babies widely expressed COX-2 immunoreactivity, as did periventricular large vessels in preterms. A number of brain cells (mature and immature cortical, periventricular and basal ganglia neurons, and oligodendrocytes of the cerebral white matter in brains from term neonates) also expressed COX-2. The present findings suggest that COX-2 may take part in enhancing neonatal brain damage via different mechanisms, such as those involving excitotoxicity and production of reactive oxygen species.

Toti, T., DE FELICE, C., Schurfeld, K., Stumpo, M., Bartolommei, S., Lombardi, F., et al. (2002). Cyclooxygenase-2 immunoreactivity in the ischemic neonatal human brain. An autopsy study. JOURNAL OF SUBMICROSCOPIC CYTOLOGY AND PATHOLOGY, 33(3), 245-249.

Cyclooxygenase-2 immunoreactivity in the ischemic neonatal human brain. An autopsy study

DE FELICE, C.;SCHURFELD, K.;BARTOLOMMEI, S.;LOMBARDI, F.;PETRAGLIA, F.;BUONOCORE, G.
2002-01-01

Abstract

Cyclooxygenase-2 (COX-2) is known to be expressed in rat brain and up-regulated by ischemia. The administration of COX inhibitors before as well as soon after the ischemic insult reduces the extension of cerebral damage in rats. Overexpression of COX-2 has also been shown in the ischemic brain of adult human patients, while no information concerning COX-2 expression in neonatal ischemia is available. Intrapartum asphyxia and perinatal brain injury may result in cerebral palsy, mental retardation or epilepsy. COX-2 expression in the brain of neonates delivered after severe birth asphyxia was investigated using immunohistochemistry. Meningeal vessel walls of term and preterm babies widely expressed COX-2 immunoreactivity, as did periventricular large vessels in preterms. A number of brain cells (mature and immature cortical, periventricular and basal ganglia neurons, and oligodendrocytes of the cerebral white matter in brains from term neonates) also expressed COX-2. The present findings suggest that COX-2 may take part in enhancing neonatal brain damage via different mechanisms, such as those involving excitotoxicity and production of reactive oxygen species.
2002
Toti, T., DE FELICE, C., Schurfeld, K., Stumpo, M., Bartolommei, S., Lombardi, F., et al. (2002). Cyclooxygenase-2 immunoreactivity in the ischemic neonatal human brain. An autopsy study. JOURNAL OF SUBMICROSCOPIC CYTOLOGY AND PATHOLOGY, 33(3), 245-249.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/29300
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