Green Tea Catechins and Their Oxidative Protection in the Rat Eye

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Kai On Chu, Kwok Ping Chan, Chi Chiu Wang, Ching Yan Chu, Wai Ying Li, Kwong Wai Choy, Michael Scott Rogers and Chi Pui Pang*

Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong Eye Department of Obstetrics and Gynecology, Prince of Wales Hospital, Shatin, New Territories, Hong Kong.

Hospital, Kowloon, Hong Kong

J. Agric. Food Chem., 2010, 58 (3), pp 15231534 DOI: 10.1021/jf9032602 Publication Date (Web): January 19, 2010 Copyright 2010 American Chemical Society *Address correspondence to this author at the Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, 3/F, Hong Kong Eye Hospital, 147K Argyle Street, Kowloon, Hong Kong [telephone (852) 27623169; fax (852) 27159490; e-mail cppang@cuhk.edu.hk].

Section: Pharmacology

Abstract

Catechins, active constituents of green tea, are well-known antioxidative natural products. It was proposed that green tea extract (GTE) consumption could benefit the eye, and the pharmacokinetics of catechins and oxidation status in rat eye were investigated after oral administration. SpragueDawley rats were fed GTE and sacrificed at different time intervals. Their eyes were dissected into cornea, lens, retina, choroid-sclera, vitreous humor, and aqueous humor for analysis of catechins and 8-epi-isoprostane by HPLC-ECD and GC-NCI-MS, respectively. Catechins were differentially distributed in eye tissues. Gallocatechin was present at the highest concentration in the retina, 22729.4 4229.4 pmol/g, and epigallocatechin in aqueous humor at 602.9 116.7 nM. The corresponding area-under-curves were 207,000 pmol h/g and 2035.0 531.7 nM h, respectively. The time of maximum concentration of the catechins varied from 0.5 to 12.2 h. Significant reductions in 8-epi-isoprostane levels were found in the compartments except the choroid-sclera or plasma, indicating antioxidative activities of catechins in these tissues.
Survey of Ophthalmology Volume 52, Issue 6, Supplement, November 2007, Pages S174-S179

doi:10.1016/j.survophthal.2007.08.013 | How to Cite or Link Using DOI

Cited By in Scopus (16)

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Is There More to Glaucoma Treatment Than Lowering IOP?

Maneli Mozaffarieh MD, Josef Flammer MD

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University Eye Clinic, Basel, Switzerland

Available online 12 November 2007.

Abstract
Classic glaucoma treatment focuses on intraocular pressure (IOP) reduction. Better knowledge of the pathogenesis of the disease has opened up new therapeutical approaches. Whereas most of these new avenues of treatment are still in the experimental phase, others, such as magnesium, gingko, salt and fludrocortisone, are already used by some physicians. Blood pressure dips can be avoided by intake of salt or fludrocortisone. Vascular regulation can be improved locally by carbonic anhydrase inhibitors, and systemically with magnesium or with low doses of calcium channel blockers. Experimentally, glaucomatous optic neuropathy can be prevented by inhibition of astrocyte activation, either by blockage of epidermal growth factor receptor or by counteracting endothelin. Glaucomatous optic neuropathy can also be prevented by nitric oxide-2 synthase inhibition. Inhibition of matrix metalloproteinase-9 inhibits apoptosis of retinal ganglion cells and tissue remodeling. Upregulation of heat shock proteins protects the retinal ganglion cells and the optic nerve head. Reduction of oxidative stress especially at the level of mitochondria also seems to be protective. This can be achieved by gingko; dark chocolate; polyphenolic flavonoids occurring in tea, coffee, or red wine; anthocyanosides found in bilberries; as well as by ubiquinone and melatonin. Key words: activation of astrocytes; autoregulation; heat shock protein; metalloproteinase; neuroprotection; nitricoxide synthase 2; oxidative stress; systemic blood pressure; vascular regulation
Brain Research Volume 1198, 10 March 2008, Pages 141-152

doi:10.1016/j.brainres.2007.12.015 | How to Cite or Link Using DOI

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Research Report

Orally administered epigallocatechin gallate attenuates retinal neuronal death in vivo and light-induced apoptosisin vitro
Bo Zhanga, Dario Ruscianob, Neville N. Osbornea,
,

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Nuffield Laboratory of Ophthalmology, Walton Street, Oxford OX2 6AW, UK SIFI, Lavinaio-Aci S. Antonio, Catania, Italy

Accepted 6 December 2007. Available online 15 December 2007.

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. Keywords: Retina; Light insult; Ischemic insult; Oral administration; Epigallocatechin gallate
Brain Research Volume 1159, 23 July 2007, Pages 40-53

doi:10.1016/j.brainres.2007.05.029 | How to Cite or Link Using DOI

Cited By in Scopus (29)

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Research Report

Epigallocatechin gallate, an active ingredient from green tea, attenuates damaging influences to the retina caused by ischemia/reperfusion
Bo Zhanga, Rukhsana Safaa, Dario Ruscianob, Neville N. Osbornea,
,

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Nuffield Laboratory of Ophthalmology, Walton Street, Oxford OX2 6AW, UK SIFI, Lavinaio-Aci S. Antonio, Catania, Italy

Accepted 12 May 2007. Available online 26 May 2007.

Abstract
The aim of this study was to examine whether the antioxidant epigallocatechin gallate (EGCG), a catechin-base flavonoid derived from green tea protects retina neurones in situ from ischemia/reperfusion andin vitro from an oxidative stress insult of hydrogen peroxide (H2O2). Similar results were obtained when rats were injected by two different regimes of EGCG. Ischemia was delivered by raising the intraocular pressure above the systolic blood pressure (120 mm Hg) generally for 45 min. The electroretinogram (ERG) was measured prior to ischemia and 5 days after reperfusion. Rats were killed 7 days after ischemia and processed for immunohistochemistry and for determining of mRNA and protein levels by RT-PCR and electrophoresis/western blotting, respectively. In addition, optic nerves 7 days after ischemia were subjected to protein analysis. Ischemia/reperfusion caused a significant

reduction in the a- and b-wave amplitudes of the ERGs, a decrease in retinal ganglion cell and photoreceptor specific proteins and mRNAs, an increase in retinal caspase-3 mRNA and protein, an increase in retinal caspase-8 mRNA, an increase in retinal GFAP protein and mRNA and a decrease in optic nerve proteins associated with ganglion cell axons. All these changes were significantly counteracted by EGCG. Moreover, EGCG clearly blunted ischemia/reperfusion-induced changes in the localisation of retinal Thy-1 and ChAT immunoreactivities. EGCG also significantly reduced the apoptosis to retinal ganglion cells (RGC-5 cells) in culture caused by H2O2. The results of the study demonstrate that EGCG provides protection to retinal neurones from oxidative stress and ischemia/reperfusion. Keywords: Retina; Ischemia; Neuroprotection; Epigallocatechin gallate