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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| Format: | Article |
| Language: | English |
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MDPI AG
2023-04-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/9/7804 |
| _version_ | 1797602497480622080 |
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| author | Robert Puls Clarissa von Haefen Christoph Bührer Stefanie Endesfelder |
| author_facet | Robert Puls Clarissa von Haefen Christoph Bührer Stefanie Endesfelder |
| author_sort | Robert Puls |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-11T04:16:51Z |
| format | Article |
| id | doaj.art-2005d07a689c4f0faa33dc3628b90aba |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T04:16:51Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-2005d07a689c4f0faa33dc3628b90aba2023-11-17T23:00:50ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-04-01249780410.3390/ijms24097804Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile RatRobert Puls0Clarissa von Haefen1Christoph Bührer2Stefanie Endesfelder3Department of Neonatology, Charité—Universitätsmedizin Berlin, 13353 Berlin, GermanyDepartment of Anesthesiology and Intensive Care Medicine, Charité—Universitätsmedizin Berlin, 13353 Berlin, GermanyDepartment of Neonatology, Charité—Universitätsmedizin Berlin, 13353 Berlin, GermanyDepartment of Neonatology, Charité—Universitätsmedizin Berlin, 13353 Berlin, GermanyThe 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.https://www.mdpi.com/1422-0067/24/9/7804hyperoxiaoxidative stresscerebellumdexmedetomidinepostnatal developing brainnewborn rat |
| spellingShingle | Robert Puls Clarissa von Haefen Christoph Bührer Stefanie Endesfelder Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat International Journal of Molecular Sciences hyperoxia oxidative stress cerebellum dexmedetomidine postnatal developing brain newborn rat |
| title | Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat |
| title_full | Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat |
| title_fullStr | Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat |
| title_full_unstemmed | Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat |
| title_short | Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat |
| title_sort | dexmedetomidine protects cerebellar neurons against hyperoxia induced oxidative stress and apoptosis in the juvenile rat |
| topic | hyperoxia oxidative stress cerebellum dexmedetomidine postnatal developing brain newborn rat |
| url | https://www.mdpi.com/1422-0067/24/9/7804 |
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