Effectiveness of Polyphenols on Perinatal Brain Damage: A Systematic Review of Preclinical Studies.
Paula Brielle PontesAna Elisa ToscanoDiego Cabral LacerdaEulália Rebeca da Silva AraújoPaulo César Trindade da CostaSwane Miranda AlvesJosé Luiz de Brito AlvesRaul Manhães-de-CastroPublished in: Foods (Basel, Switzerland) (2023)
Polyphenol supplementation during early life has been associated with a reduction of oxidative stress and neuroinflammation in diseases caused by oxygen deprivation, including cerebral palsy, hydrocephaly, blindness, and deafness. Evidence has shown that perinatal polyphenols supplementation may alleviate brain injury in embryonic, fetal, neonatal, and offspring subjects, highlighting its role in modulating adaptative responses involving phenotypical plasticity. Therefore, it is reasonable to infer that the administration of polyphenols during the early life period may be considered a potential intervention to modulate the inflammatory and oxidative stress that cause impairments in locomotion, cognitive, and behavioral functions throughout life. The beneficial effects of polyphenols are linked with several mechanisms, including epigenetic alterations, involving the AMP-activated protein kinase (AMPK), nuclear factor kappa B (NF-κB), and phosphoinositide 3-kinase (PI3K) pathways. To highlight these new perspectives, the objective of this systematic review was to summarize the understanding emerging from preclinical studies about polyphenol supplementation, its capacity to minimize brain injury caused by hypoxia-ischemia in terms of morphological, inflammatory, and oxidative parameters and its repercussions for motor and behavioral functions.
Keyphrases
- brain injury
- early life
- oxidative stress
- nuclear factor
- protein kinase
- cerebral ischemia
- systematic review
- subarachnoid hemorrhage
- toll like receptor
- cerebral palsy
- randomized controlled trial
- dna damage
- ischemia reperfusion injury
- diabetic rats
- induced apoptosis
- dna methylation
- meta analyses
- lps induced
- case control
- gene expression
- signaling pathway
- lipopolysaccharide induced
- stem cells
- cell therapy
- traumatic brain injury
- white matter
- inflammatory response
- risk assessment
- immune response
- cognitive impairment
- endoplasmic reticulum stress
- blood brain barrier
- resting state
- metabolic syndrome
- cell proliferation
- heat shock protein