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.
Highlights
Neonatal hypoxic-ischemic (HI) is a common cause of death and long-term neurological injuries in newborns [1]
The results showed that the number of transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells had been notably decreased with vitexin pretreatment (60.65 ± 21.73 cells; P
We suggest for the first time that pretreatment with vitexin may inhibit neuronal apoptosis in neonatal hypoxic-ischemic injury by suppression of calcium/calmodulin dependent protein kinase II (CaMKII)
Summary
Neonatal hypoxic-ischemic (HI) is a common cause of death and long-term neurological injuries in newborns [1]. The mechanisms underlying HI brain damage involve excitotoxicity, apoptosis, and inflammation [2]. In this process, due to absence of oxygen reaching the brain, anaerobic glycolysis is rapidly initiated, it will result in an inadequate supply of energy [3]. As result of energy failure, a battery of biochemical events will occur. Overproduction of reactive oxygen species (ROS) and activation of nitric oxide synthase may be leading to excitotoxicity in neuron [4]. It seems that inhibition of Ca2+ toxicity may be neuroprotective for HI brain injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
