Compound of icariin, astragalus, and puerarin mitigates iron overload in the cerebral cortex of Alzheimer's disease mice

Increasing evidence indicates that disruption of normal iron homeostasis may contribute to pathological development of Alzheimer's disease. Icariin, astragalus, and puerarin have been shown to suppress iron overload in the cerebral cortex and improve spatial learning and memory disorders in Alzheimer's disease mice, although the underlying mechanism remains unclear. In the present study, APPswe/PS1 Delta E9 transgenic mice were administered icariin, astragalus, and puerarin (120, 80, and 80 mg/kg, respectively, once a day, for 3 months). Iron levels were detected by flame atomic absorption spectroscopy. Interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels were measured in the cerebral cortex by enzyme linked immunosorbent assay. Glutathione peroxidase and superoxide dismutase activity and malondialdehyde content were determined by colorimetry. Our results demonstrate that after treatment, iron levels and malondialdehyde content are decreased, while glutathione peroxidase and superoxide dismutase activities are increased. Further, interleukin-1 beta, interleukin-6, and tumor necrosis factor-a levels were reduced. These results confirm that compounds of icariin, astragalus, and puerarin may alleviate iron overload by reducing oxidative stress and the inflammatory response.