Green tea is neuroprotective in diabetic retinopathy

• Published in: Investigative ophthalmology & visual science Vol. 54; no. 2; p. 1325
• Main Authors: Silva, Kamila C, Rosales, Mariana A B, Hamassaki, Dania E, Saito, Kelly C, Faria, Aline M, Ribeiro, Patrícia A O, Faria, José B Lopes de, Faria, Jacqueline M Lopes de
• Format: Journal Article
• Language: English
• Published: United States 15.02.2013
• Subjects: Animals; Antioxidants - pharmacology; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - metabolism; Diabetic Retinopathy - etiology; Diabetic Retinopathy - metabolism; Diabetic Retinopathy - prevention & control; Electroretinography; Male; Oxidative Stress - drug effects; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Retina - metabolism; Retina - pathology; Tea - chemistry
• ISSN: 1552-5783; 1552-5783
• DOI: 10.1167/iovs.12-10647

Green tea (GT), widely studied for its beneficial properties in protecting against brain ischemia, is a rich source of polyphenols, particularly (-)-epigallocatechin gallate (EGCG). The results presented here demonstrate the beneficial effects of GT in diabetic retinas and in retinal cells under diabetic conditions. Diabetes was induced in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats. Treatment animals received GT orally for 12 weeks. A vehicle was administered orally to the control animals. The protective effects of GT were also evaluated in Müller and in ARPE-19 cells. In diabetic rats, there was an increase in the expression of glial fibrillary acidic protein (GFAP), oxidative retinal markers, and glutamine synthetase levels. In addition, there was a decrease in occludin and glutamate transporter and receptor. Diabetic SHR also demonstrated blood-retinal barrier breakdown and impaired electroretinography results. Müller cells exposed to high-glucose medium produced higher levels of reactive oxygen species (ROS) and glutamine synthetase but reduced levels of glutathione, glutamate transporter, and glutamate receptor. Similarly, ARPE-19 cells exhibited increased ROS production accompanied by decreased expression of claudin-1 and glutamate transporter. Treatment with GT fully restored all the above-mentioned alterations in diabetic animals as well as in retinal cells. GT protected the retina against glutamate toxicity via an antioxidant mechanism. These findings reveal a novel mechanism by which GT protects the retina against neurodegeneration in disorders such as diabetic retinopathy.