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Vitexin protects against hypoxic-ischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinase II and apoptosis signaling in the neonatal mouse brain.
- Source :
-
Oncotarget [Oncotarget] 2017 Apr 11; Vol. 8 (15), pp. 25513-25524. - Publication Year :
- 2017
-
Abstract
- Neonatal hypoxic-ischemic is a major cause of death and disability in neonates. In this study, we suggest for the first time that pretreatment with vitexin may suppress a pro-apoptotic signaling pathway in hypoxic-ischemic neuronal injury in neonates by inhibition of the phosphorylation of Ca2+/Calmodulin-dependent protein kinase II. Here we found that vitexin pretreatment reduced brain infarct volume in a dose-dependent manner. In addition, vitexin decreased the number of TUNEL-positive cells and brain atrophy. Furthermore, vitexin improved neurobehavioral outcomes. Vitexin also reduced oxygen glucose deprivation-induced neuronal injury and calcium entry. Vitexin pretreatment increased the Bcl-2/Bax protein ratio and decreased phosphorylation of Ca2+/Calmodulin-dependent protein kinase II and NF-κB, cleaved caspase-3 protein expression 24 hours after injury. Our data indicate that pretreatment with vitexin protects against neonatal hypoxic-ischemic brain injury and thus has potential as a treatment for hypoxic-ischemic brain injury.
- Subjects :
- Animals
Animals, Newborn
Atrophy
Brain Infarction etiology
Brain Infarction metabolism
Brain Infarction pathology
Calcium metabolism
Cell Death drug effects
Cell Survival drug effects
Cells, Cultured
Disease Models, Animal
Dose-Response Relationship, Drug
Glucose metabolism
Hypoxia-Ischemia, Brain drug therapy
Hypoxia-Ischemia, Brain pathology
Mice
NF-kappa B metabolism
Neurons drug effects
Neurons metabolism
Oxygen metabolism
Apigenin pharmacology
Apoptosis drug effects
Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism
Hypoxia-Ischemia, Brain metabolism
Neuroprotective Agents pharmacology
Signal Transduction drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1949-2553
- Volume :
- 8
- Issue :
- 15
- Database :
- MEDLINE
- Journal :
- Oncotarget
- Publication Type :
- Academic Journal
- Accession number :
- 28424420
- Full Text :
- https://doi.org/10.18632/oncotarget.16065