Aminoguanidine protects against apoptosis of retinal ganglion cells in Zucker diabetic fatty rats.

AIM The inhibition of advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) mediated downstream signaling pathways have been suggested to have retinoprotective actions in diabetic retinopathy. Herein, we examined the protective effects of aminoguanidine (AG), an AGEs inhibitor, on diabetes-induced injury of retinal ganglion cells in the Zucker diabetic fatty (ZDF) rats. MATERIALS AND METHODS Seven-week-old male ZDF rats were treated with AG (50 mg/kg body weight) once a day orally for 13 weeks. Serum and vitreous concentration of AGEs were examined. Expressions of AGEs and its receptor (RAGE) were assessed by immunohistochemistry. Southwestern histochemistry was used to detect activated nuclear factor (NF)-κB. RESULTS At the end of the study, vitreal levels of AGEs were significantly reduced in ZDF rats treated with AG. Similary, immunohistochemical analysis showed that AG significantly reduced the positive areas for AGEs and RAGE. Furthermore, AG strongly inhibited the loss of retinal ganglion cells by apoptosis. AG also suppressed the activation of to NF-κB. CONCLUSIONS Our results suggest that AG has retinoprotective properties through not only direct inhibition of AGEs formation but also downregulation of NF-κB.