Gypenoside XVII alleviates early diabetic retinopathy by regulating Müller cell apoptosis and autophagy in db/db mice.

Diabetic retinopathy (DR) is a widespread vision-threatening disease in working people. Müller cells are important glial cells that participate in the blood retinal barrier and promote the maintenance of retinal physiological and structural homeostasis. Müller cell apoptosis and autophagy play an important role in the pathogenesis of DR. Gypenoside XVII (Gyp-17) exerts strong antiapoptotic and autophagic activities. However, the effect of Gyp-17 on DR and its mechanism of action have not been elucidated. This study explored the effect of Gyp-17 on early DR and Müller cell injury in db/db mice. Blood glucose and blood lipids were measured. Optical coherence tomography and fundus fluorescein angiography were applied to detect retinal thickness and vascular leakage, respectively. Hematoxylin eosin staining assessed the pathological changes of the retina. Retinal oxidative environment and cell apoptosis and autophagy were monitored using commercial kits, immunofluorescence, and Western blot assays. Results showed that Gyp-17 exerted no significant effect on blood glucose and lipid levels but maintained normal retinal permeability, physiological structure, high anti-oxidative enzyme expression, and the thickness of the inner nuclear layer compared with the model group. Moreover, Western blot analysis and TUNEL assay indicated that Gyp-17 significantly decreased pro-apoptotic-related protein expression and increased pro-autophagy-related protein expression compared with the model group. Immunofluorescence colocalization exhibited that the regulating action of Gyp-17 may focus on Müller cells. These data strongly demonstrate that Gyp-17 prevents early DR by decreasing apoptosis and increasing autophagy in Müller cells. Gyp-17 may be a candidate drug for early DR therapy.