Protective effect of epigallocatechin gallate on brain damage after transient middle cerebral artery occlusion in rats

Abstract

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.