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- W4366991266 endingPage "7804" @default.
- W4366991266 startingPage "7804" @default.
- W4366991266 abstract "The risk of oxidative stress is unavoidable in preterm infants and increases the risk of neonatal morbidities. Premature infants often require sedation and analgesia, and the commonly used opioids and benzodiazepines are associated with adverse effects. Impairment of cerebellar functions during cognitive development could be a crucial factor in neurodevelopmental disorders of prematurity. Recent studies have focused on dexmedetomidine (DEX), which has been associated with potential neuroprotective properties and is used as an off-label application in neonatal units. Wistar rats (P6) were exposed to 80% hyperoxia for 24 h and received as pretreatment a single dose of DEX (5µg/kg, i.p.). Analyses in the immature rat cerebellum immediately after hyperoxia (P7) and after recovery to room air (P9, P11, and P14) included examinations for cell death and inflammatory and oxidative responses. Acute exposure to high oxygen concentrations caused a significant oxidative stress response, with a return to normal levels by P14. A marked reduction of hyperoxia-mediated damage was demonstrated after DEX pretreatment. DEX produced a much earlier recovery than in controls, confirming a neuroprotective effect of DEX on alterations elicited by oxygen stress on the developing cerebellum." @default.
- W4366991266 created "2023-04-27" @default.
- W4366991266 creator A5070665957 @default.
- W4366991266 creator A5076056908 @default.
- W4366991266 creator A5086599742 @default.
- W4366991266 creator A5089834699 @default.
- W4366991266 date "2023-04-25" @default.
- W4366991266 modified "2023-10-01" @default.
- W4366991266 title "Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat" @default.
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- W4366991266 doi "https://doi.org/10.3390/ijms24097804" @default.