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Increased oxidative stress, which can lead to the retinal pigment epithelium (RPE) cell death by inducing ATP depletion and DNA repair, is believed to be a prominent pathology in age-related macular degeneration (AMD). In the present study, we showed that and 0.1 mM nicotinamide adenine dinucleotide (NAD + ) administration significantly blocked RPE cell death induced by 300 μM H 2 O 2 . Further investigation showed that H 2 O 2  resulted in increased intracellular ROS level, activation of PARP-1 and subsequently necrotic death of RPE cells. Exogenous NAD +  administration significantly decreased intracellular and intranuclear ROS levels in H 2 O 2 -treated RPE cells. In addition, NAD +  administration to H 2 O 2 -treated RPE cells inhibited the activation of PARP-1 and protected the RPE cells against necrotic death. Moreover, exogenous NAD +  administration up-regulated autophagy in the H 2 O 2 -treated RPE cells. Inhibition of autophagy by LY294002 blocked the decrease of intracellular and intranuclear ROS level. Besides, inhibition of autophagy by LY294002 abolished the protection of exogenous NAD +  against H 2 O 2 -induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD +  administration suppresses H 2 O 2 -induced oxidative stress and protects RPE cells against PARP-1 mediated necrotic death through the up-regulation of autophagy. The results suggest that exogenous NAD +  administration might be potential value for the treatment of AMD.

Exogenous NAD+ decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy