Berberine suppresses advanced glycation end products‐associated diabetic retinopathy in hyperglycemic mice.

Berberine suppresses advanced glycation end products-associated diabetic retinopathy in hyperglycemic mice To determine whether the inhibitory effect of BBR on VEGF production was mediated by its inhibition of STAT3, we transfected a plasmid encoding constitutively activated STAT3 mutant (STAT3C) into BBR-treated HRECs. The cytotoxicity of BBR on HREC cells was measured by MTT assay and the inhibitory concentration (IC)20 of BBR was calculated as 25.11 M. Doses of BBR lower than the IC20 were considered non-toxic to HREC cells. The formation of advanced glycation end products (AGEs) and AGEs-related signalling pathway activation in the retina leads to the initiation of retinopathy in diabetic patients.1 In this study, we identified the natural compound berberine (BBR) as a potent AGEs inhibitor that significantly suppressed AGEs formation and its related TLR4/STAT3/VEGF signalling pathway in the retina endothelial cells, thus contributing to its therapeutic effect on diabetic retinopathy (DR). [Extracted from the article]