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 signal - ing pathways have been suggested to have retinoprotective actions in diabetic retinopathy. Herein, we examined the protective effects of aminoguanidine (AG), an AGEs inhibitor, on dia - betes-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 immunohistochem - istry. Southwestern histochemistry was used to detect activated nuclear factor (NF)- κB. RESULTS: At the end of the study, vitreal lev - els of AGEs were significantly reduced in ZDF rats treated with AG. Similary, immunohisto - chemical 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 sup - pressed the activation of to NF- κB. CONCLUSIONS: Our results suggest that AG has retinoprotective properties through not on - ly direct inhibition of AGEs formation but also downregulation of NF- κB.