Mechanism Of Early Diabetic Retinal Ganglion Cell Degeneration And Drug Intervention

Diabetic Retinopathy(DR)is a neurodegenerative disorder which is mainly caused by the apoptosis of retinal Ganglion Cells(RGCs).However,its pathogenesis has not yet been elucidated,and its high incidence is also urgently needed to find drugs for intervention.We have investigated the protective effect of Bismaltolato oxidovanadium(IV)-[VO(ma)2](BMOV)on the retina of high-fat diet(HFD)mice and the protective effects of notoginsenoside(CSPN)on sodium palmitate(PA)stimulated RGC-5 cells.First,we established an early HFD-induced diabetic mouse model and used two different concentrations of BMOV for drug intervention.After 8 weeks of treatment,we used OGTT,visual evoked potentials,paraff-in sections,immunofluorescence and other techniques to detect visual acuity and synaptic protein expression in mice to evaluate the efficacy of BMOV In vitro experiments,we chose the differentiated RGC-5 cells to perform our experiments.PA was used to simulate the high-fat environment in DR and CSPN was used for intervention.Western Blot,cellular immunofluorescence,CCK8 and other experiments were used to detect apoptosis to evaluate the efficacy of CSPN.The experimental results showed that after 16 weeks of high-fat diet,mouse blood glucose increased,visual reaction sensitivity decreased,synaptic protein loss,and RGC cells showed significant apoptosis.But there was a significant improvement in the BMOV treatment group,and high doses are more effective than low doses.The treatment of 400?g/mL PA for 24 hours caused the collapse of RGC-5 cytoskeleton,loss of synaptic proteins,endoplasmic reticulum stress,and apoptosis,while CSPN can suppress this process.