Purpose: Oxidative injury to the retinal pigment epithelium (RPE) has been proposed to play a contributing role in age-related macular degeneration (AMD). Exposure to solar ultraviolet (UV) radiation is believed to cause the production of reactive oxygen species (ROS), which may cause oxidative damage to RPE cells. Studies have shown that (-)-epigallocatechin gallate (EGCG), an abundant and active component in green tea, can protect several cell types from oxidative stress. It may be useful in the prevention of early AMD.
Methods: To determine whether EGCG protects RPE cells from UVA-induced damage, we used a cell viability assay to determine the viability of UVA-treated cells. Intracellular H(2)O(2) levels were measured by flow cytometry. Western blotting was used to detect UVA-induced signaling pathways.
Results: The results indicated that EGCG inhibits UVA-induced RPE cell death. In addition, intracellular H(2)O(2) generation in RPE cells irradiated by UVA was inhibited by EGCG in a concentration-dependent manner. EGCG also inhibited UVA-induced extracullar signal-regulated kinase (ERK) and c-jun-NH2 terminal kinase (JNK) activation in RPE cells while a higher concentration of EGCG had an inhibitory effect on UVA-induced p38 activation. Finally, we investigated cyclooxygenase-2 (COX-2) expression in RPE cells exposed to UVA radiation, and EGCG was found to also have inhibited UVA-induced COX-2 expression.
Conclusions: Taken together, our results demonstrate that EGCG inhibits UVA-induced H(2)O(2) production, mitogen-activating protein kinase activation, and expression of COX-2. Moreover, it enhances RPE cell survival after UVA exposure. This suggests EGCG is effective in preventing UVA-induced damage in RPE cells and may be suitable for further developments as a chemoprotective factor for the primary prevention of early AMD.