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Neuroprotective fractalkine in fetal alcohol syndrome
Robin Roberson1, Thea Kuddo, Ines Benassou
1Unit on Perinatal and Developmental Neurobiology, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. robersor@mail.nih.gov
Objective:
Neuroprotective peptides (NAP+SAL) can prevent some alcohol-induced damage in fetal alcohol syndrome(FAS). Fractalkine, a chemokine constitutively expressed in the CNS reduces neuronal death from activated microglia. Using a model of FAS we evaluated if fractalkine is altered and if NAP+SAL work through fractalkine.
Study Design:
Using a FAS model, C57BL6/J-mice were treated on gestational day 8 with alcohol (0.03 mL/g), placebo or alcohol+peptides. Embryos were harvested after 6h(E8) and 10 days later(E18). Fractalkine was measured in the protein lysate (Luminex xMAP). Statistical analysis included Kruskal-Wallis.
Results:
Fractalkine was significantly elevated at 6h (median 341 pg/ml, range 263-424 pg/ml) vs. controls (median 228 pg/ml, range 146-332 pg/ml; P<.001). NAP+SAL prevented the alcohol-induced increase (median 137, range 97-255 pg/ml, P<.001). At E18, fractalkine levels were similar in all groups (P=0.7).
Conclusion:
Prenatal alcohol exposure acutely elevates fractalkine, perhaps in an effort to counter the alcohol toxicity. Pre-treatment with NAP+SAL prevents the acute increase in fractalkine.
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