The present study was performed to evaluate the protective effects of
icariin on cognitive function in a hypoxia-induced neonatal
epilepsy rat model. Neonatal
epilepsy was induced in rat pups on postnatal day (PD) 20 by induction of
hypoxia for 15 minutes. Rats were treated intraperitoneally with
icariin at 75 mg/kg 1 hour before the induction of
hypoxia. The effects of
icariin were examined by estimating seizure stage, cognitive function and parameters of electroencephalography (EEG) in this neonatal
epilepsy rat model. Parameters of oxidative stress and expression of
proteins were examined in the brain tissue of the neonatal
epilepsy rat model by histopathological study and Western blotting analysis, respectively. The results of this study suggest that treatment with
icariin ameliorates the changes in seizure stage, number of
seizures and parameters of EEG in
hypoxia-induced neonatal
epilepsy rats. Oxidative stress and apoptosis were decreased in the brain tissue of the
icariin treatment group compared to the
hypoxia group. Moreover, treatment with
icariin ameliorated the altered expression of
glutamate ionotropic
receptor AMPA type subunit 2 (GluR2) and extracellular receptor
kinase (ERK I/II)
proteins in the brain tissue of
hypoxia-induced
epilepsy rats. Histopathological study also showed that
icariin treatment improved the histopathology of brain tissue of
hypoxia-induced
epilepsy rats. In conclusion, the results of the present study suggest that
icariin protects against neuronal injury and improves cognitive function in
hypoxia-induced neonatal
epilepsy rats by modulating the GluR2/ERK I/II pathway.