U83836E inhibits retinal neurodegeneration in early-stage streptozotocin-induced diabetic rats.

Oxidative stress plays a role in the pathogenesis of neurodegeneration in diabetic retinopathy (DR). However, whether an excellent reactive oxygen species scavenger, U83836E, inhibits the neurodegeneration in DR remains uncertain. This study is aimed at clarifying the effects of U83836E on DR. Two weeks after streptozotocin (STZ) injection, diabetic rats and control animals were assigned at random to receive U83836E or vehicle for 2 weeks. Transmission electron microscopy and electroretinography were used to observe the changes in retina ultrastructure and electrophysiological function, respectively; superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were measured using a spectrometer. STZ-induced diabetic rats showed obvious vacuolation and many swollen mitochondria in the retinal ganglion cells of the retina, and reduced amplitudes of b-waves and oscillatory potentials. Concomitantly, there was a decrease in SOD activity and increase in MDA levels. These changes were inhibited by U83836E. These results suggest that U83836E improves neurodegeneration in DR and possesses a great potential for the treatment of DR.