Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat

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 cogn...

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Bibliographic Details
Main Authors: Bührer, C. (Author), Endesfelder, S. (Author), Puls, R. (Author), von Haefen, C. (Author)
Format: Article
Language:English
Published: MDPI 2023
Subjects:
Online Access:View Fulltext in Publisher
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LEADER 02288nam a2200253Ia 4500
001 10.3390-ijms24097804
008 230529s2023 CNT 000 0 und d
020 |a 16616596 (ISSN) 
245 1 0 |a Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat 
260 0 |b MDPI  |c 2023 
856 |z View Fulltext in Publisher  |u https://doi.org/10.3390/ijms24097804 
856 |z View in Scopus  |u https://www.scopus.com/inward/record.uri?eid=2-s2.0-85159326895&doi=10.3390%2fijms24097804&partnerID=40&md5=73e126091b6990ab7352e8ec920dde64 
520 3 |a 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. © 2023 by the authors. 
650 0 4 |a cerebellum 
650 0 4 |a dexmedetomidine 
650 0 4 |a hyperoxia 
650 0 4 |a newborn rat 
650 0 4 |a oxidative stress 
650 0 4 |a postnatal developing brain 
700 1 0 |a Bührer, C.  |e author 
700 1 0 |a Endesfelder, S.  |e author 
700 1 0 |a Puls, R.  |e author 
700 1 0 |a von Haefen, C.  |e author 
773 |t International Journal of Molecular Sciences