Oxidative-induced retinal degeneration is attenuated by epigallocatechin gallate.
The aim of this investigation was to determine whether an ingredient of green tea, epigallocatechin gallate (EGCG) could attenuate oxidative stress-induced degeneration of the retina as occurs in age-related macular degeneration (AMD) and glaucoma. Initial in vitro studies on brain membranes showed that EGCG was approximately 10 times more potent than trolox (vitamin E analogue) at attenuating lipid peroxidation caused by the nitric oxide donor, sodium nitroprusside (SNP). Subsequent immunohistochemical studies revealed that following an intraocular injection of SNP retinal photoreceptors are affected. This was supported by electroretinogram (ERG) recordings which showed both the a- and b-wave amplitudes to be significantly reduced. RT-PCR and Western blotting techniques showed that SNP caused a significant decrease in photoreceptor-specific markers (RET-P1, rhodopsin kinase), an increase in the cell death marker caspase-3, and no change in the ganglion cell specific markers, neurofilament (NF-L) and Thy-1. Importantly, when EGCG was co-injected, the detrimental effects to the retina caused by SNP were significantly blunted. The conclusion reached from this study is that EGCG is a powerful antioxidant and when injected into the eye with SNP attenuated the detrimental influence of SNP to retinal photoreceptors. Since oxidative stress has been implicated in retinal diseases like AMD and glaucoma this study provides "proof of principle" for the idea that daily intake of EGCG may help individuals suffering from retinal diseases where oxidative stress is implicated.
Zhang
B
B
Nuffield Laboratory of Ophthalmology, Oxford University, Walton Street, Oxford OX2 6AW, UK.
Osborne
N N
NN
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004596:Electroretinography / Q000379:methods; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry / Q000379:methods; D020287:In Situ Nick-End Labeling / Q000379:methods; D015227:Lipid Peroxidation / Q000187:drug effects; D016900:Neurofilament Proteins / Q000235:genetics / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D018384:Oxidative Stress; D011493:Protein Kinase C / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D012162:Retinal Degeneration / Q000188:drug therapy* / Q000209:etiology; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D017299:Rod Opsins / Q000235:genetics / Q000378:metabolism; D025603:Sensory Rhodopsins / Q000235:genetics / Q000378:metabolism; D018800:Thy-1 Antigens / Q000235:genetics / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D016900:Neurofilament Proteins; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D017299:Rod Opsins; D025603:Sensory Rhodopsins; D018800:Thy-1 Antigens; D005680:gamma-Aminobutyric Acid; D002392:Catechin; C045651:epigallocatechin gallate; D002795:Choline O-Acetyltransferase; D011493:Protein Kinase C; D053148:Caspase 3