Green Tea Extract Ameliorates Ischemia-Induced Retinal Ganglion Cell Degeneration in Rats

• Published in: Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-10
• Main Authors: Pang, Chi-Pui, Sun, Xinghuai, Ng, Tsz Kin, Yang, Qichen, Huang, Shaofen, Chen, Shao-Lang, Xu, Yanxuan, Liang, Jiajian, Chen, Yuhong, Xu, Ciyan, Yang, Yaping, Cen, Ling-Ping
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Caspase 3 - metabolism; Cell Survival - drug effects; Cytokines; Drug therapy; Female; Ganglion; Glaucoma; Green tea; Health aspects; Inflammation; Ischemia; Kinases; Laboratory animals; Neurosciences; Oxidative stress; Oxidative Stress - drug effects; p38 Mitogen-Activated Protein Kinases - genetics; p38 Mitogen-Activated Protein Kinases - metabolism; Pharmacology; Photoreceptors; Plant Extracts - chemistry; Protective Agents - chemistry; Protective Agents - pharmacology; Protective Agents - therapeutic use; Proteins; Rats; Rats, Inbred F344; Reperfusion Injury - complications; Reperfusion Injury - pathology; Retina; Retinal Degeneration - etiology; Retinal Degeneration - metabolism; Retinal Degeneration - prevention & control; Retinal Ganglion Cells - cytology; Retinal Ganglion Cells - metabolism; Rodents; Sodium; Superoxide Dismutase - genetics; Superoxide Dismutase - metabolism; Survival analysis; Tea; Tea - chemistry; Tea - metabolism; Tumor necrosis factor-TNF
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2019/8407206

Purpose. Oxidative stress induced by reduced blood circulation is a critical pathological damage to retinal ganglion cells (RGCs) in glaucoma. We previously showed that green tea extract (GTE) and its catechin constituents alleviate sodium iodate-induced retinal degeneration in rats. Here, we investigated the therapeutic effect of GTE on ischemia-induced RGC degeneration in rats. Methods. RGC degeneration was induced by ischemic reperfusion in adult Fischer F344 rats. Green tea extract (Theaphenon E) was intragastrically administered 4 times within 48 hours after ischemia. RGC survival, pupillary light reflex, expressions of cell apoptosis, oxidative stress, and inflammation-related proteins were studied. Results. Ischemic reperfusion significantly induced apoptotic RGCs, RGC loss, and larger constricted pupil area compared to the untreated normal rats. Expressions of activated caspase-3 and caspase-8, Sod2, and inflammation-related proteins as well as p38 phosphorylation were significantly upregulated in the ischemia-injured rats. Compared to the saline-fed ischemic rats, significantly higher number of surviving RGCs, less apoptotic RGCs, and smaller constricted pupil area were observed in the GTE-fed ischemic rats. GTE also reduced the increased protein expressions caused by ischemic injury but enhanced the Jak phosphorylation in the retina. Notably, green tea extract did not affect the survival of RGCs in the uninjured normal rats. Conclusions. In summary, GTE offers neuroprotection to RGCs under ischemic challenge, suggesting a potential therapeutic strategy for glaucoma and optic neuropathies.