Ibrain fulaxin protects cortical neurons from neonatal hypoxic-ischemic encephalopathy by upregulating vascular endothelial growth factor

Neonatal hypoxic-ischemic encephalopathy (NHIE) is a perinatal neonatal brain injury disease caused by hypoxia, manifested by cell damage, metabolic disorders, vascular dysregulation disorders, and decreased

The objective of this study was to explore the potential mechanism

To assess the expression and localization of VEGF in HI rat neurons, the researchers performed VEGF and NeuN immunofluorescence double staining

Figure 1 Effect of xanthanin on the growth of neurons expressing VEGF

Members of the caspase-3 and Caspase-7 families of cysteine aspartate protease (Caspase) are known to be executive proteins for apoptosis^[3].

Figure 2 Changes in factors and mRNA levels interacting with VEGF

In summary, in this study, the researchers found that HI injury can lead to severe nerve damage and cerebral infarction, and the protein chip data revealed differential expression of VEGF in cortical, hippocampal, and lung tissues and its co-localization with neurons

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References

[1] Ballot D E, Rakotsoane D, Cooper P A, Ramdin T D, Chirwa T, Pepper M S.
A prospective observational study of developmental outcomes in survivors of neonatal hypoxic ischaemic encephalopathy in south africa.
S Afr Med J.
2020; 110(4):308-312.

[2] Fernandez-Lopez D, Martinez-Orgado J, Casanova I, Bonet B, Leza J C, Lorenzo P, Moro M A, Lizasoain I.
Immature rat brain slices exposed to oxygen-glucose deprivation as an in vitro model of neonatal hypoxic-ischemic encephalopathy.
J Neurosci Methods.
2005; 145(1-2):205-212.

[3] Deng C, Li J, Li L, Sun F, Xie J.
Effects of hypoxia ischemia on caspase-3 expression and neuronal apoptosis in the brain of neonatal mice.
Exp Ther Med.
2019; 17(6):4517-4521.

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