AI Article Synopsis
- OGD caused reduced cell viability, increased apoptosis, and lower expression of the glutamate receptor subunit GluR2, along with decreased potassium channel currents.
- Genistein was found to partially counteract these negative effects, suggesting it could help prevent neuronal apoptosis in hypoxic/ischemic conditions by influencing GluR2 expression and potassium currents.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.etap.2017.01.022 | DOI Listing |
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