Consumption of green tea (GT) is associated with decreased incidences of diverse diseases in humans. Epigallocatechin-3-gallate (EGCG) and EGC are major catechins of green tea. Hyperglycemia is thought to be a primary factor in the development of diabetic neuropathy. Neuronal cell loss is a general phenomenon of diabetic neuropathy. Therefore, we examined the preventive effects of green tea extracts (GTE), EGCG, and EGC against high glucose-induced death of PC12 neuronal, cells derived from the rat adrenal medulla. In present study, high glucose resulted in decreased cell viability and stimulated lipid peroxide [LPO] formation, and [3H]-glutamate uptake. Treatment with 10 mg/mL of GTE prevented high glucose-induced cell death, lipid peroxide formation, and [3H]-glutamate uptake in PC12 cells. In addition, treatment with EGCG and EGC prevented high glucose-induced cell death, LPO formation, and glutamate uptake. Thus, we found that green tea protected against hyperglycemia-induced cell death, and its main action was mediated through reduction of oxidative stress and glutamate uptake in neuron cells. In conclusion, GTE prevented high glucose-induced neuron cell death by decreasing oxidative stress and glutamate uptake in PC12 cells.