Conclusion
Aucubin can protect RGCs in diabetic rats, inhibit RGC apoptosis, and reduce oxidative stress and inflammatory response, and 10 mg/kg aucubin showed optimal efficacy. The mechanism may be related to the inhibition of the p38MAPK signaling pathway.
Methods
A rat model of diabetes mellitus was created by single intraperitoneal injection of 55 mg/kg of streptozotocin. Rats were treated with intraperitoneal injection of 1, 5, and 10 mg/kg aucubin or 5 μg/kg p38MAPK inhibitor SB203580, once a day, for 28 consecutive days. Body weight, blood glucose, morphological changes, count and apoptosis of RGCs, p38MAPK signaling pathway, apoptosis-related proteins, oxidative stress indices, and inflammatory factors were observed and compared among the groups.
Objective
To explore the role of aucubin in regard to injured retinal ganglion cells (RGCs) in diabetic rats and its mechanism.
Results
Aucubin and SB203580 reduced the abnormality of the photoreceptor layer, bipolar cell layer and RGCs. Aucubin significantly reduced body weight, fasting blood glucose, RGC apoptosis rate, p38MAPK protein phosphorylation level, protein expression of Caspase 3 and Bax, vascular endothelial growth factors (interleukin-1β, intercellular adhesion molecule-1 and tumor necrosis factor-α) and malondialdehyde levels, and increased RGC count and protein expression of Bcl-2 and Bcl-2/Bax (P < 0.05).