Abstract
Neonatal hypoxic-ischemic (HI) brain injury is one of the major drawbacks of mortality and causes significant short/long-term neurological dysfunction in newborn infants worldwide. To date, due to multifunctional complex mechanisms of brain injury, there is no well-established effective strategy to completely provide neuroprotection. Although therapeutic hypothermia is the proven treatment for hypoxic-ischemic encephalopathy (HIE), it does not completely chang outcomes in severe forms of HIE. Therefore, there is a critical need for reviewing the effective therapeutic strategies to explore the protective agents and methods. In recent years, it is widely believed that there are neuroprotective possibilities of natural compounds extracted from plants against HIE. These natural agents with the anti-inflammatory, anti-oxidative, anti-apoptotic, and neurofunctional regulatory properties exhibit preventive or therapeutic effects against experimental neonatal HI brain damage. In this study, it was aimed to review the literature in scientific databases that investigate the neuroprotective effects of plant extracts/plant-derived compounds in experimental animal models of neonatal HI brain damage and their possible underlying molecular mechanisms of action.
Highlights
Hypoxia-ischemia (HI) is regarded as one of the major drawbacks of brain damage in the neonates and infants
In addition to introducing neonatal HI brain damage and its pathophysiology, in this study, we aimed to review the literature in scientific databases that investigate the protective effects of plant extracts or their constituents in experimental animal models of neonatal HI brain damage and their possible underlying mechanisms of action
Adjusted the expression of the mRNA and protein of the PI3K/protein kinase B (Akt)/GSK3β pathway, inhibited the expression of NR2B protein, and regulated apoptosis mediators. These results demonstrated that OMT exerts neuroprotection against neonatal hypoxic-ischemic brain damage (HIBD) via regulating apoptosis, NR2B downregulation, and activation of the PI3K/Akt/GSK3β signaling pathway [203,204]
Summary
Hypoxia-ischemia (HI) is regarded as one of the major drawbacks of brain damage in the neonates and infants. Neonatal hypoxic-ischemic brain damage (HIBD) (synonymous with hypoxic-ischemic encephalopathy (HIE)) is the main drawback of newborn deaths and irretrievable and long-lasting neurodevelopmental disabilities in the sufferers [1]. Epilepsy, mental retardation, motor and cognitive deficits, learning and behavioral disabilities, and other severe neurological disorders were regularly observed in the sufferers based on brain injury grade [3,4]. In infants with mild HIE, the death probability is 10% and the risk of neurodevelopmental disorders is 30%, while 60% of infants with severe HIE are at risk of death and all sufferers risk exposure to remarkable disabilities. The rate of incidence in the very low birth weight infants is 60% of all live births
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