Abstract
ObjectiveTo investigate the permeability of β-NGF through blood–brain-barrier (BBB) in neonatal and adult rats, and the spatial distribution of β-NGF in different brain regions in hypoxic-ischemic (HI) and normal neonatal rats.MethodsTo investigate the overall permeability of β-NGF through BBB, β-NGF labeled with I125 was injected into adult rats, neonatal rats and HI neonatal rats via tail vein. The radioactivity of brain tissue and blood was examined and analyzed 30 min after injection. Also, brain regions including the basal forebrain, frontal cortex, hippocampus, hypothalamus, cerebellum, bulbus olfactorius and hypophysis, of all the rats were dissected and radioactivity was examined to investigate the spatial specificity of NGF permeation through BBB.ResultsStatistically significant results were observed in I125-β-NGF contents in brain tissues of adult rats group, neonatal rats group and HI neonatal rats group (P < 0.05). Compared to the HI neonatal rats’ brain with the highest I125-β-NGF contents, normal neonatal rats ranks the second while the adult rats were the lowest. While for the spatial specificity examination part, I125-β-NGF in both HI group and control group were widely distributed in basal forebrain, frontal cortex, hippocampus, cerebellum and bulbus olfactorius. But the radioactivity in frontal cortex, hippocampus and cerebellum of HI groups are statistically higher than control groups (P < 0.05).Conclusionβ-NGF can more easily penetrate the BBB of newborn rats than adult rats via peripheral venous administration and this effect can be enhanced by HI insult. Also, this HI-induced permeation of β-NGF through BBB is more obvious in frontal cortex, hippocampus and cerebellum.
Highlights
Hypoxic ischemic encephalopathy, named as hypoxic ischemic encephalopathy (HIE), is one type of brain damage caused by prolonged insufficient blood and oxygen supply (Fatemi et al 2009)
We studied the permeability of β-nerve growth factor (NGF) through BBB and examined the absorption and distribution of NGF in newborn rats with hypoxic-ischemic brain damage, neonatal rats and adult rats in healthy condition
As we apply NGF in the neonatal HI group, we found the apoptosis in the hippocampus of neonatal HI group with NGF injection is much milder compared to control group with only I125 injection
Summary
Named as HIE, is one type of brain damage caused by prolonged insufficient blood and oxygen supply (Fatemi et al 2009). Studies (Cortazzo et al 1996; Nguyen et al 2010; Satoh et al 1999) found that nerve growth factor (NGF) can prevent apoptosis of neuron cells including the neural crest cells (Cortazzo et al 1996; Satoh et al 1999) and hippocampal cells (Nguyen et al 2010). Lindvall et al (1994) found that brain damage can lead to an increase of endogenous NGF, which may contribute to nerve protection effect (Fan et al 2007). NGF is one of the nerve cell growth regulatory factors involved in the proliferation, maintenance and survival in the neural cells, and is maintained at a moderately low level in the brain. In spite of the protective role of endogenous NGF in hypoxic insults or other damage of brain, the endogenous NGF is still quite limited and is difficult to exert long-lasting protection from the damage (O’Driscoll and Gorman 2005; Lindvall et al 1992)
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