Icariin is a prenylated
flavonol glycoside derived from the Chinese herb Epimedium sagittatum that exerts a variety of pharmacological activities and shows promise in the treatment and prevention of
Alzheimer's disease. In this study, we investigated the
neuroprotective effects of
icariin against
amyloid beta protein fragment 25-35 (Aβ 25-35) induced neurotoxicity in cultured rat
pheochromocytoma PC12 cells and explored potential underlying mechanisms. Our results showed that
icariin dose-dependently increased cell viability and decreased Aβ 25-35-induced apoptosis, as assessed by MTT assay and
Annexin V/
propidium iodide staining, respectively. Results of western blot analysis revealed that the selective
phosphatidylinositol 3-kinase (PI3K) inhibitor
LY294002 suppressed
icariin-induced Akt phosphorylation, suggesting that the protective effects of
icariin are associated with activation of the PI3K/Akt signaling pathway.
LY294002 also blocked the
icariin-induced downregulation of proapoptotic factors Bax and
caspase-3 and upregulation of antiapoptotic factor Bcl-2 in Aβ 25-35-treated PC12 cells. These findings provide further evidence for the clinical efficacy of
icariin in the treatment of
Alzheimer's disease.