title: Epigallocatechin-3-gallate reduces retinal ischemia/reperfusion injury by attenuating neuronal nitric oxide synthase expression and activity.
abstract: Retinal ischemia/reperfusion (IR) injury causes profound tissue damage, especially retinal ganglion cell death. The aims of the study were twofold: (1) to investigate the benefits of epigallocatechin-3-gallate (EGCG), the major catechin found in tea, after IR challenge, and (2) to elucidate the mechanism of EGCG inhibition of nitric oxide synthase (NOS) expression. Wistar female rats were divided into four groups: normal control, EGCG with sham operation, retinal IR, and EGCG with IR groups. EGCG (50mg/kg) was administered by intraperitoneal injection 30 min before the experiment. IR injury to a rat's retina was induced by raising intraocular pressure to 150 mmHg for 60 min. With EGCG pretreatment, retinal ganglion cell death from IR was reduced by approximately 10% 3 days afterward. EGCG significantly downregulated IR-induced glial fibrillary acidic protein expression. EGCG treatment also reduced TUNEL-positive cells after IR in the inner retina as well as IR-induced lipid peroxidation. Histological analyses showed fewer neuronal NOS and nicotinamide adenine dinucleotide phosphate diaphorase-positive cells in the retina after IR with EGCG administration. Therefore, EGCG is effective in protecting retinal ganglion cells from IR challenge by ameliorating retinal nitrosactive stress and by regulating cell death through apoptotic pathways.
authors.affiliation: Department of Ophthalmology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
authors.forename: Pai-Huei
authors.initials: PH
authors.lastname: Peng
authors.forename: Mei-Lan
authors.initials: ML
authors.lastname: Ko
authors.forename: Chau-Fong
authors.initials: CF
authors.lastname: Chen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016923:Cell Death / Q000187:drug effects; D004353:Drug Evaluation, Preclinical / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D015227:Lipid Peroxidation / Q000187:drug effects; D009249:NADP / Q000037:antagonists & inhibitors / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012164:Retinal Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000473:pathology
chemical_list: D000975:Antioxidants; D004791:Enzyme Inhibitors; D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D009249:NADP; D002392:Catechin; C045651:epigallocatechin gallate; D019001:Nitric Oxide Synthase