Effect And Mechanism Of Salt Intake On Experimental Diabetic Retinopathy

Diabetic retinopathy(DR)is an important ocular complication of diabetes mellitus,and inflammation is an important factor in the pathogenesis of DR.As processed food consumption increased,the overall salt intake of the population increased significantly.Dietary recommendations to reduce salt intake have been introduced in many clinical guidelines because the association between high salt intake and hypertension may exacerbate diabetes complications.NaCl is the main component of salt and an essential nutrient in People's Daily life.Sodium ion is the main cation in extracellular fluid to maintain the electric gradient of cell membrane and is the most important electrolyte in body fluid regulation.Therefore,long-term changes in NaCl intake may affect the normal function of cells,leading to physiological and even pathological changes.Studies have found that excessive salt intake can promote the secretion of inflammatory factors and the formation of chronic inflammation,aggravating autoimmune diseases and target organ injury.Inflammation plays a critical role in the progression of DR,but the role of high salt in the pathogenesis of DR is unclear.We established a STZ-induced mouse model of type 1 diabetic retinopathy,and observed the changes in retinal function and pathological changes by changing salt intake,and observed the effects of different salt concentrations on BMDMs and HRECs inflammation in a high-glucose environment.The results of animal experiments showed that salt intake had no significant effect on serum ion concentration,blood pressure and blood osmotic pressure of DR mice.High salt diet increased sodium ion concentration in DR vitreous fluid,while low salt diet decreased sodium ion concentration in DR vitreous fluid.Changes in salt intake can result in abnormal changes in retinal photoreceptor cell structure.Activated retinal microglia in DR mice,but reduced synaptic phagocytosis.Among them,high salt diet can also damage synaptic integrity;Changes in salt intake induced local retinal inflammation in DR mice and activated NLRP3 inflammatory bodies in DR mice.The results of cell experiments showed that the expression of TNF-?,IL-1? and P-P65 in BMDMs and HRECs and NLRP3 and Caspase-1 in BMDMs and HRECs were increased in both high and low salt conditions.After MCC950 intervention,NLRP3,Caspase-1 and IL-1? expressions in BMDMs and HRECs high-salt and low-salt groups were significantly decreased.In conclusion,our research from the overall level and cell level,confirmed the high salt and low salt can promote the occurrence of DR by activation of NLRP3 inflammasome,both low and high salt promoting DR progress.Our research provides a reasonable reference for clinical patients with DR salt intake.