Epigallocatechin gallate (EGCG), a major constituent of green tea, is a potent free radical scavenger. The purpose of this study was to verify whether EGCG reduces focal ischemia/reperfusion-induced brain injury in a rat model. Male Sprague-Dawley rats were anesthetized with chloral hydrate (400 mg/kg, i.p.) and subjected to a middle cerebral artery 2 h occlusion and then a 24-h reperfusion. The EGCG (25 mg and 50 mg/kg, i.p.) or vehicle was administered immediately after reperfusion. Twenty-four hours after reperfusion, infarction size, levels of oxidative stress markers (malondialdehyde and oxidized/total glutathione ratio) in the brain and neurological deficits were evaluated. The dose of 50 mg/kg of EGCG significantly reduced the infarction volume (9.9+/-3.2%) as compared to those (45.6+/-5.3%, 34.5+/-7.8%) of the control group and the EGCG 25 mg/kg treated group (p<0.01). The dose of 50 mg/kg of EGCG significantly reduced the neurological deficit total score (5.2+/-1.7) as compared to those (9.5+/-1.2, 8.5+/-2.5) of the control group and the EGCG 25 mg/kg treated group (p<0.05). The dose of 50 mg/kg of EGCG significantly attenuated the level of malondialdehyde and the level of oxidized/total glutathione ratio (281+/-66 nmol/g and 0.48+/-0.03) as compared to the those (415+/-46 nmol/g and 0.64+/-0.05, 381+/-51 nmol/g and 0.61+/-0.06) of the control group and the EGCG 25 mg/kg treated group (p<0.05). These results demonstrate the anti-oxidant effects of EGCG (50 mg/kg) in a rat model of transient focal ischemia, which is a likely explanation for EGCG's neuroprotective effects.