Protective effect of metformin on rat diabetic retinopathy involves suppression of toll-like receptor 4/nuclear factor-k B expression and glutamate excitotoxicity.

摘要: Abstract Microvascular complications of diabetes mellitus are progressively significant reasons for mortality. Metformin (MET) is considered as the first-line therapy type 2 patients, and may be especially beneficial in cases diabetic retinopathy although precise mechanisms MET action not fully elucidated. The current study was designed to inspect antioxidant modulatory actions on DRET streptozotocin-induced rats. effect toll-like receptor 4/nuclear factor kappa B (TLR4/NFkB), inflammatory burden glutamate excitotoxicity assessed. Twenty-four male rats were assigned four experimental groups: (1) Vehicle group, (2) Diabetic control: developed by injection streptozotocin (60 mg/kg, i.p.). (3&4) Diabetic + MET group: left 9 weeks without treatment then received oral 100 200 mg/kg 6 weeks. Retinal samples utilized biochemical, histological, immunohistochemical electron microscopic studies. administration significantly decreased retinal level insulin growth suppressed induced increase malondialdehyde, glutamate, tumor necrosis factor-α vascular endothelial (VEGF). Further, mRNA expression NFkB, TLR4 findings shed light MET’s efficacy an adjuvant hinder development retinopathy, at least partly, via inhibition oxidative stress-induced NFkB/TLR4 pathway suppression excitotoxicity.