17β-estradiol ameliorates oxidative stress and blue light-emitting diode-induced retinal degeneration by decreasing apoptosis and enhancing autophagy.

PURPOSE

This study aimed to assess the effects of 17β-estradiol (βE) on blue light-emitting diode (LED)-induced retinal degeneration (RD) in rats and hydrogen peroxide (HO)-induced retinal pigment epithelium cell injury in humans and elucidate the protective mechanism of βE underlying these processes.

METHODS

Female ovariectomized (OVX) rats were intravitreally injected with βE2 before blue LED exposure (3,000 lux, 2 hours). Retinal function and morphology were assayed via electroretinogram (ERG) and H&E, respectively. Cell viability was assayed using the Cell Counting Kit-8. Cell ROS were measured using dichlorofluorescein fluorescence. Apoptosis was evaluated by TUNEL and Annexin V/propidium iodide staining. Gene expression and protein expression were quantified using quantitative real-time RT-PCR, Western blotting, and immunohistochemistry. Autophagosomes were examined by electron microscopy.

RESULTS

Female OVX rats were exposed to blue LED, inducing RD. βE significantly prevented the reduction in the a- and b-wave ERG amplitudes and the disruption of retinal structure, the loss of photoreceptor cells, and the decrease in the thickness of the outer nuclear layer caused by blue LED exposure. βE also decreased cell apoptosis in the retina in blue LED-induced RD. Additionally, βE reduced ROS levels and apoptosis in HO-treated human retinal pigment epithelial (ARPE-19) cells. Furthermore, βE increased the protein expression of p-Akt and Bcl-2 and decreased the protein expression of cleaved caspase-3 and Bax during blue LED-induced retinal damage and in HO-treated ARPE-19 cells. βE also increased the number of autopha-gosomes and upregulated the expression of LC3-II/LC3-I and Beclin 1 in these processes.

CONCLUSION

βE protects against blue LED-induced RD and HO-induced oxidative stress by acting as an antioxidant, and its protective mechanism might occur by reducing apoptosis and enhancing autophagy; βE may be a novel and effective therapy for age-related macular degeneration.