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Many N-methyl-d-aspartate (NMDA) receptor antagonists have been used to treat neurodegenerative diseases induced by glutamate excitotoxicity in clinics. However, the universality of the glutamic acid neurotransmitter system makes the glutamic acid receptor blockers inefficient and unsafe. Thus, regulating the downstream signaling pathway in the excitotoxicity of glutamic acid may be a more effective and safer way to antagonize the glutamic acid receptor. In this study, we investigated the effect of deferoxamine (DFO), an iron chelator, on the NMDA-induced excitotoxicity. RGC-5 cells were cultured and identified in vitro, and the NMDA-induced injury was assessed. Then the MTT assay was used to estimate the cell survival and JC-1 staining was performed to detect changes in mitochondrial membrane potential. Immunofluorescent staining and western blot analysis were used to analyze the expressions of respiratory chain proteins. It was found that DFO increased the survival rate of RGC-5 cells and that this effect was positively correlated with the concentration of DFO and the treatment time. The mitochondrial membrane potential and the expression levels of succinate dehydrogenase subunit A and cytochrome c oxidase subunit IV were also increased after DFO treatment, while NMDA reduced their expression levels. These data demonstrate that DFO has significant neuroprotective activity against NMDA-induced excitotoxicity in RGC-5 cells.

Neuroprotective effect of deferoxamine on &lt;italic&gt;N&lt;/italic&gt;-methyl-d-aspartate-induced excitotoxicity in RGC-5 cells

Neuroprotective effect of deferoxamine on <italic>N</italic>-methyl-d-aspartate-induced excitotoxicity in RGC-5 cells