Protective effects of (-)-epigallocatechin gallate on blue light-induced damage in retinoblastoma Y 79 cells by activating estrogen receptor pathway

Light-induced photoreceptor cell death can be caused by a variety of cellular mechanisms that involve oxidative stress. Therefore, the eye depends on the presence of antioxidants to protect the retina from light-induced damage. Visible light is generated by the sun as well as by a wide variety of artificial illumination sources such as light emitting diodes (LED). Excessive exposure to light would be damaging to the eye. The short-wavelength visible light between 430 nm to 500 nm (blue light) is especially associated with retina damage as evidenced by photoreceptor degeneration. Recent investigations demonstrated that estrogen receptors (ERs) have antioxidant and antiinflammatory effects on neuronal cells in brain. However, estrogen receptor (ER)-mediated effects of the (-)epigallocatechin gallate (EGCG), extracted from green tea, have not been examined extensively in photoreceptors of the eyeball. EGCG were examined for the ability to elicit ERs and ER-mediated gene expression in vitro. Our studies were demonstrated that the cell degeneration of retinoblastoma Y79 cells was observed after blue light exposure. Apoptosis related proteins, p53 and caspase-3, increased the expression after blue light illumination. After EGCG treatment, increased ER proteins production and inhibited the blue light-induced retinoblastoma Y79 cells death were investigated. These results indicated the short-wavelength visible light, such as white LED exposure, leads to retinoblastoma Y79 damage. EGCG regulates the expression of neuroprotective proteins, ER, and modulates degeneration responses in human retinoblastoma Y79 cells. [Mei-Ling Peng, Ching-Ju Lee, Chung-Liang Chien, Chun-Lan Liu, Cheng-Yu Tsai, Yang-Cheng Wen, KuangWen Tseng. Protective effects of (-)-epigallocatechin gallate on blue light-induced damage in retinoblastoma Y79 cells by activating estrogen receptor pathway. Life Sci J 2013;10(1):192-198] (ISSN:1097-8135). http://www.lifesciencesite.com. 28