title: Orally administered epigallocatechin gallate attenuates retinal neuronal death in vivo and light-induced apoptosis in vitro.
abstract: The aim of this study was to provide support for epigallocatechin gallate (EGCG), a component of green tea, to be considered in the context for neuroprotection in glaucoma, where administration by an oral route is required for adequate penetration into the retina. Ischemia was delivered to one eye of a number of rats by raising the intraocular pressure. EGCG was present in the drinking water of half of the animals 3 days before ischemia and also during the next 5 days of reperfusion. The electroretinograms (ERGs) of both eyes from all rats were recorded before ischemia and 5 days following ischemia. Seven days after ischemia retinas from both eyes of all rats were either analysed for the localisation of various antigens or extracts prepared for analysis for the level of specific proteins and mRNAs. Ischemia/reperfusion to the retina affected a number of parameters. These included the localisation of Thy-1 and choline acetyltransferase, the a- and b-wave amplitudes of the ERG, the content of certain retinal and optic nerve proteins and various mRNAs. Significantly, EGCG statistically blunted many of the effects induced by ischemia/reperfusion which included the activation of caspases. These studies demonstrate conclusively that orally administered EGCG attenuates injury to the retina caused by ischemia/reperfusion where caspases were activated. Studies were also conducted on a cell line (RGC-5 cells) where it was shown that white light (1000 lx, 48 h)-induced apoptosis is caspase-independent and can be blunted by EGCG. The present studies support the view for the use of EGCG in the treatment of glaucoma based on the premise that any potential neuroprotective agent must be administered orally, have a safe profile and poses a broad spectrum of properties that allows various risk factors (that include ischemia and light) to be attenuated.
authors.affiliation: Nuffield Laboratory of Ophthalmology, Walton Street, Oxford OX2 6AW, UK.
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Dario
authors.initials: D
authors.lastname: Rusciano
authors.forename: Neville N
authors.initials: NN
authors.lastname: Osborne
mesh_terms: D000284:Administration, Oral; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002460:Cell Line; D004596:Electroretinography; D005901:Glaucoma / Q000188:drug therapy* / Q000503:physiopathology; D007511:Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008027:Light / Q000009:adverse effects; D008297:Male; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control; D012160:Retina / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D012162:Retinal Degeneration / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D018696:Neuroprotective Agents; D002392:Catechin; D020169:Caspases; C057580:gallocatechol