2023
DOI: 10.3390/ijms24097804
|View full text |Cite
|
Sign up to set email alerts
|

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

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 a… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

2023
2023
2024
2024

Publication Types

Select...
2

Relationship

1
1

Authors

Journals

citations
Cited by 2 publications
(1 citation statement)
references
References 89 publications
(128 reference statements)
0
1
0
Order By: Relevance
“…Shown in H9c2 cells under OGD/R injury as well as in CoCl 2 -induced injury to mimic hypoxia [ 71 ], both Hif1α and autophagy-related mediators are induced [ 72 ]. Compared to previous studies, DEX demonstrated a protective effect on cardiomyocytes by inhibiting ROS-induced apoptosis [ 41 ], an antioxidant effect on the developing rodent brain [ 73 ], as well as known neuroprotective mechanisms in general [ 74 , 75 ]. Li et al [ 76 ] demonstrated the protection of H9c2 cells against CoCl 2 -induced damage using the antioxidant naringin, a natural bioflavonoid, by enhancing autophagic flux via activation of the Hif1α/BNIP3 pathway.…”
Section: Discussionmentioning
confidence: 95%
“…Shown in H9c2 cells under OGD/R injury as well as in CoCl 2 -induced injury to mimic hypoxia [ 71 ], both Hif1α and autophagy-related mediators are induced [ 72 ]. Compared to previous studies, DEX demonstrated a protective effect on cardiomyocytes by inhibiting ROS-induced apoptosis [ 41 ], an antioxidant effect on the developing rodent brain [ 73 ], as well as known neuroprotective mechanisms in general [ 74 , 75 ]. Li et al [ 76 ] demonstrated the protection of H9c2 cells against CoCl 2 -induced damage using the antioxidant naringin, a natural bioflavonoid, by enhancing autophagic flux via activation of the Hif1α/BNIP3 pathway.…”
Section: Discussionmentioning
confidence: 95%