Abstract
Müller cell gliosis, with a characterization of increase in glial fibrillary acidic protein (GFAP), plays a key role in diabetic retinopathy (DR), a leading cause of blindness in people of working age. Recent studies have shown that in diabetes Müller cells produced high levels of vascular endothelial growth factor (VEGF) and pro-inflammatory cytokines. In the present study, we investigated whether GSEs protect against hyperglycemia-induced injury to Müller cells in retinal tissues and cell culture. The results showed that GSEs attenuated diabetes-induced increase in GFAP, VEGF, and inflammatory factors in the retina of streptozotocin-diabetic rats. Studies in primary Müller cells supported these findings by detecting a reduction in angiogenic and inflammatory mediators upon treatment with GSEs. We believe that GSEs may alleviate oxidative stress by increasing the expression of Nrf2-responsive antioxidant genes including HO-1 and GCLC. These data demonstrated that GSEs protect the retina against injury during DR.
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