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

• Published in: Brain research Vol. 1019; no. 1-2; pp. 47 - 54
• Main Authors: Choi, Young Bin, Kim, Yeong In, Lee, Kwang Soo, Kim, Beum Saeng, Kim, Dai Jin
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 03.09.2004; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Antioxidant; Biological and medical sciences; Catechin - analogs & derivatives; Catechin - pharmacology; Catechin - therapeutic use; EGCG; Free radical; Hypoxia, Brain - drug therapy; Hypoxia, Brain - pathology; Hypoxia, Brain - prevention & control; Infarction, Middle Cerebral Artery - drug therapy; Infarction, Middle Cerebral Artery - pathology; Infarction, Middle Cerebral Artery - prevention & control; Ischemia; Lipid Peroxidation - drug effects; Lipid Peroxidation - physiology; Male; Medical sciences; Middle cerebral artery occlusion; Neuropharmacology; Neuroprotective agent; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Pharmacology. Drug treatments; Rat; Rats; Rats, Sprague-Dawley; Ischemia; Rat; Antioxidant; EGCG; Middle cerebral artery occlusion; Free radical; Nervous system diseases; Rodentia; Cardiovascular disease; Neuroprotective agent; Radical scavenger; Cerebral disorder; Encephalon; Vascular disease; Vertebrata; Experimental disease; Polyphenol; Mammalia; Animal; Central nervous system disease; Plant origin; Green tea; Cerebrovascular disease
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2004.05.079

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.