Abstract
Asphyctic brain injury is a major cause of neuronal inflammation in the perinatal period. Fetal asphyctic preconditioning has been shown to modulate the cerebral inflammatory cytokine response, hereby protecting the brain against asphyctic injury at birth. This study was designated to examine the effects of perinatal asphyxia and fetal asphyctic preconditioning on the inflammatory cytokine response in the cerebellum. Fetal asphyxia was induced at embryonic day 17 by clamping the uterine vasculature for 30 min. At term birth, global perinatal asphyxia was induced by placing the uterine horns in saline for 19 min. Pro- and anti-inflammatory cytokine expression were assessed by real-time PCR and immunohistochemistry in cerebella of newborn rats. We found that tumor necrosis factor alpha and interleukin-10 mRNA were increased 12 h after fetal asphyxia, while the inflammatory cytokine response was decreased 96 h postfetal asphyxia. When applied as preconditioning stimulus, fetal asphyxia attenuates the cerebellar cytokine response. These results indicate that sublethal fetal asphyxia may protect the cerebellum from perinatal asphyxia-induced damage via inhibition of inflammation.
Highlights
Perinatal asphyxia, affecting 2–4 neonates per 1,000 births, is a major birth concern
We have shown that the inflammatory cytokine expression might play an important role in this preconditioning phenomenon [10]. As knowledge of these pathways is of outmost importance for the development of neuroprotective strategies, we examined whether inflammatory cytokine expression was increased in cerebella of rats that had experienced perinatal asphyxia during Caesarean section birth, and, if so, whether fetal asphyctic preconditioning can modulate this inflammatory response in the cerebellum
We demonstrate that fetal asphyxia per se downregulates the inflammatory cytokine responses in the cerebellum at time of birth when a perinatal asphyctic episode occurs
Summary
Perinatal asphyxia (hypoxia–ischemia), affecting 2–4 neonates per 1,000 births, is a major birth concern. Infants affected by global asphyxia may develop hypoxic-ischemic encephalopathy (HIE) with neurodevelopmental abnormalities in childhood, presenting as learning disability, seizure activity, motor impairment, and, in the most severe cases, death [2, 3]. Many of these deficits may be related to cerebellar injury, since the cerebellum is one of the brain regions playing an important role in the control of motor functions and in higher cognitive functions and behavioral changes [4]. Previous studies have shown that cerebellar lesions caused by perinatal asphyxia greatly affect locomotor activity [6, 7]
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