Investigation into injury effects and related mechanisms of advanced glycation end-products on cortical neurons

Recent studies showed that advanced glycosylation end-products (AGEs) is toxic to central neuron system. However, the precise molecular mechanism of such toxicity has not yet been fully clarified. In the present study, we determined the injury effect of AGEs on cortical neurons cells. In vitro functional analysis using the ultraviolet spectrophotometer method revealed that AGEs increased the concentration of hydroxyl radical and malondialdehyde (MDA) in a dose-dependent way, and the effect was largely blocked by AGEs antibody (Ab-RAGE). Confocal laser microscopy showed that AGEs induced apoptosis of cultured neurons cells by its receptor(RAGE). These results indicated that increasing of hydroxyl radical and MDA levels, as well as inducing apoptosis are major mechanisms of AGEs mediated central neuron injury.