LAUSR

Purpose To investigate the protective effects of sulforaphane, an Nrf2 activator, on streptozotocin (STZ)-induced diabetic retinopathy. Methods 8 wk male C57BL/6 mice were intraperitoneally injected with streptozotocin (STZ, 45 mg/kg) for 5 consective days. Animals with fasting blood glucose higher than 13.89 mmol/L were considered diabetes and used for further study. Two weeks after STZ injection, animals were intraperitoneally injected with sulforaphane (12.5 mg/kg) for 8 wks, 3 times per week and retinas were harvested at the tenth-week. Reactive oxygen species (ROS) in retina were detected by DHE staining. The expression of heme oxygenase-1 (HO-1) and Nox2 in retina was detected by Western blotting. Immunofluorescent staining was used to detect the expression of RNA binding protein with multiple splicing (RBPMS)and choline acetyl transferase (ChAT), which could specifically mark the retinal ganglion cells (RGCs) and amacrine cells (ACs), respectively. Acellular capillaries in retina were observed by using periodic acid-Schiff and hematoxylin staining. Results The fasting blood glucose of the mice injected with STZ was increased rapidly, accompanied by significantly decreased body weight. STZ-injection induced increased ROS generation, increased RGCs and ACs loss, and increased formation of acellular capillaries, which could all be reversed by SF treatment. Meanwhile, HO-1 and Nox2 expression were increased by STZ-injection. SF treatment could further enhance STZ-induced HO-1 expression, whereas decreased STZ-induced Nox2 expression. Conclusions SF treatment could protect mice retina from STZ-induced oxidative stress and cellular damage, possibly through the activation of Nrf2 antioxidant pathway and inhibition of Nox2 expression.