Icariin inhibits corticosterone-induced apoptosis in hypothalamic neurons via the PI3-K/Akt signaling pathway.

Excessive corticosterone (CORT) is acknowledged to induce neuronal damage in a number of regions of the brain, particularly the hippocampus, the main area implicated in depression. However, little research has been conducted on alterations to hypothalamic neurons in depression and the cellular and molecular basis for these changes. In the present study, we aimed to determine whether CORT causes apoptosis in primary cultured hypothalamic neurons, and to investigate the protective effects of icariin, an active natural ingredient from the Chinese plant, Epimedium sagittatum Maxim. Our study demonstrates that exposure of hypothalamic neurons to CORT causes a significant loss in viability, a significant decrease in mitochondrial membrane potential, an increase in caspase-3 activity, an elevation in intracellular reactive oxygen species elevation and decreased superoxide dismutase activity. However, pretreatment of cells with icariin prior to CORT exposure was identified to noticeably suppress these CORT-induced events. Furthermore, icariin may prevent CORT-induced cell death via activation of the PI3-K/Akt pathway. In conclusion, icariin is able to prevent CORT-induced hypothalamic cell apoptosis via activation of the PI3-K/Akt pathway.