Genistein inhibits hypoxia, ischemic-induced death, and apoptosis in PC12 cells

- Genistein inhibits hypoxic-ischemia-caused apoptosis/death in PC12 Cell.
- Genistein reverses Decrease in K+ efflux in hypoxic-ischemic PC12 Cell.
- Genistein reverses down-regulation of GluR2 in hypoxic-ischemic PC12 Cell.

A hypoxia/ischemia neuronal model was established in PC12 cells using oxygen-glucose deprivation (OGD). OGD-induced neuronal death, apoptosis, glutamate receptor subunit GluR2 expression, and potassium channel currents were evaluated in the present study to determine the effects of genistein in mediating the neuronal death and apoptosis induced by hypoxia and ischemia, as well as its underlying mechanism. OGD exposure reduced the cell viability, increased apoptosis, decreased the GluR2 expression, and decreased the voltage-activated potassium currents. Genistein partially reversed the effects induced by OGD. Therefore, genistein may prevent hypoxia/ischemic-induced neuronal apoptosis that is mediated by alterations in GluR2 expression and voltage-activated potassium currents.