Inhibiting NADPH oxidase protects against long-term memory impairment induced by neonatal sevoflurane exposure in mice

Abstract

Background: Neonatal exposure to anaesthetics such as sevoflurane has been reported to result in behavioural deficits in rodents. However, while oxidative injury is thought to play an underlying pathological role, the mechanisms of neurotoxicity remain unclear. In the present study, we investigated whether the NADPH oxidase inhibitor apocynin protects against longterm memory impairment produced by neonatal sevoflurane exposure in mice. Methods: Postnatal day six mice were divided into four groups; (1) non-anaesthesia, (2) intraperitoneal apocynin (50 mg kg

Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice

“…Sevoflurane anesthesia was performed as described previously [19]. Briefly, postnatal day-6 mice were placed in a humid chamber immediately after removal from the maternal cage.…”

“…Western blot analysis of the forebrain protein lysate was performed as described previously [19]. The forebrains were removed quickly after 6 h of sevoflurane anesthesia.…”

“…Immunohistochemistry was performed as described previously [19]. The tissues were perfused after 6 h of sevoflurane anesthesia.…”

“…Volatile anesthetics at clinical concentrations induced neuronal apoptosis and cognitive disorders in neonatal and aged rodents [13–19]. We previously studied neuronal apoptosis and cognitive dysfunction in mice with neonatal sevoflurane exposure [14, 19]. That neuronal damage was due to exposure of the immature central nervous system [20].…”

“…The developing brain is vulnerable to sevoflurane exposure [14, 15, 19]. We postulated that sugammadex coadministration with neonatal sevoflurane may exacerbate neuronal apoptosis due to changes in BBB integrity.…”