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10.1038/srep26322 http://scihub22266oqcxt.onion/10.1038/srep26322 C4886526!4886526 !27240523     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27240523 &cmd=llinks): Failed to open stream: HTTP request failed! 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Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy |pdf=|usr=}}{{27240523 }} gab.com Text Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27240523 #FOAvip 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??M H2O2. Further investigation showed that H2O2 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 H2O2-treated RPE cells. In addition, NAD(+) administration to H2O2-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 H2O2-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 H2O2-induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD(+) administration suppresses H2O2-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. Twit Text FOAVip Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27240523 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27240523 #FOAvip English Wikipedia <ref>{{Cite pmid|27240523 }}</ref> Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy #MMPMID27240523 Zhu Y ; Zhao KK ; Tong Y ; Zhou YL ; Wang YX ; Zhao PQ ; Wang ZY Sci Rep 2016[May]; 6 (ä): 26322 PMID27240523 show ga 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??M H2O2. Further investigation showed that H2O2 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 H2O2-treated RPE cells. In addition, NAD(+) administration to H2O2-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 H2O2-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 H2O2-induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD(+) administration suppresses H2O2-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. |Autophagy/drug effects [MESH] |Cell Survival/drug effects [MESH] |Cells, Cultured [MESH] |Chromones/pharmacology [MESH] |Humans [MESH] |Hydrogen Peroxide/toxicity [MESH] |Macular Degeneration/drug therapy/metabolism/pathology [MESH] |Models, Biological [MESH] |Morpholines/pharmacology [MESH] |NAD/*metabolism/pharmacology [MESH] |Necrosis [MESH] |Oxidants/toxicity [MESH] |Oxidative Stress/drug effects [MESH] |Poly (ADP-Ribose) Polymerase-1/metabolism [MESH] |Reactive Oxygen Species/metabolism [MESH] |Retinal Pigment Epithelium/drug effects/*metabolism/*pathology [MESH]Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated (epmc).pdf DeepDyve Pubget Overpricing