Study · In vitro (cells) · 2011
16 resultsPittelli M, Felici R, Pitozzi V, Giovannelli L, Bigagli E, Cialdai F, Romano G, Moroni F, Chiarugi A
Molecular pharmacology14 Sept 2011Cited by 100 (Europe PMC)
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Text rights: Publisher copyright. Results still quote short attributed sentences.
13 results from studies that gave the peptide. No result from this study comes from people.
In cell lines or primary cultures, exogenous NAD increased intracellular NAD content.
In plain wordsIn cells, exogenous NAD increased intracellular NAD content.
n: not reported in source
Cell lines or primary culturesSource sentences
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, NAD precursors could not reproduce the effects of exogenous NAD.
In plain wordsIn cells, NAD precursors could not reproduce the effects of exogenous NAD.
n: not reported in source
Cell lines or primary culturesSource sentences
NAD precursors could not reproduce the effects of eNAD
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In the cell incubation medium, NAD precursors were not detected during exogenous NAD exposure.
In plain wordsIn lab tests, NAD precursors were not detected in the medium containing exogenous NAD.
n: not reported in source
Cell lines or primary culturesSource sentences
NAD precursors could not reproduce the effects of eNAD, and they were not found in the incubating medium containing eNAD, thereby suggesting direct cellular eNAD uptake.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells exposed to exogenous NAD, mitochondrial NAD increased.
In plain wordsIn cells, exogenous NAD increased mitochondrial NAD.
n: not reported in source
Cell lines or primary culturesSource sentences
We found that in mitochondria of cells exposed to eNAD, NAD and NADH as well as oxygen consumption and ATP production were increased.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells exposed to exogenous NAD, mitochondrial NADH increased.
In plain wordsIn cells, exogenous NAD increased mitochondrial NADH.
n: not reported in source
Cell lines or primary culturesSource sentences
We found that in mitochondria of cells exposed to eNAD, NAD and NADH as well as oxygen consumption and ATP production were increased.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells exposed to exogenous NAD, mitochondrial oxygen consumption increased.
In plain wordsIn cells, exogenous NAD increased mitochondrial oxygen consumption.
n: not reported in source
Cell lines or primary culturesSource sentences
We found that in mitochondria of cells exposed to eNAD, NAD and NADH as well as oxygen consumption and ATP production were increased.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells exposed to exogenous NAD, mitochondrial ATP production increased.
In plain wordsIn cells, exogenous NAD increased mitochondrial ATP production.
n: not reported in source
Cell lines or primary culturesSource sentences
We found that in mitochondria of cells exposed to eNAD, NAD and NADH as well as oxygen consumption and ATP production were increased.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, DNA repair remained unaltered during exogenous NAD exposure.
In plain wordsIn cells, exogenous NAD did not change DNA repair.
n: not reported in source
Cell lines or primary culturesSource sentences
Conversely, DNA repair, a well known NAD-dependent process, was unaltered upon eNAD exposure.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, exogenous NAD conferred significant protection from staurosporine-induced apoptosis.
In plain wordsIn cells, exogenous NAD protected against apoptosis induced by staurosporine.
n: not reported in source
Cell lines or primary culturesSource sentences
We also report that eNAD conferred significant cytoprotection from apoptosis triggered by staurosporine, C2-ceramide, or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, exogenous NAD conferred significant protection from C2-ceramide-induced apoptosis.
In plain wordsIn cells, exogenous NAD protected against apoptosis induced by C2-ceramide.
n: not reported in source
Cell lines or primary culturesSource sentences
We also report that eNAD conferred significant cytoprotection from apoptosis triggered by staurosporine, C2-ceramide, or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, exogenous NAD conferred significant protection from apoptosis induced by N-methyl-N'-nitro-N-nitrosoguanidine.
In plain wordsIn cells, exogenous NAD protected against apoptosis induced by N-methyl-N'-nitro-N-nitrosoguanidine.
n: not reported in source
Cell lines or primary culturesSource sentences
We also report that eNAD conferred significant cytoprotection from apoptosis triggered by staurosporine, C2-ceramide, or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, exogenous NAD reduced staurosporine-induced loss of mitochondrial membrane potential.
In plain wordsIn cells, exogenous NAD reduced mitochondrial membrane potential loss induced by staurosporine.
n: not reported in source
Cell lines or primary culturesSource sentences
In particular, eNAD reduced staurosporine-induced loss of mitochondrial membrane potential and ensuing caspase activation.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In cells, exogenous NAD reduced caspase activation following staurosporine-induced loss of mitochondrial membrane potential.
In plain wordsIn cells, exogenous NAD reduced caspase activation after staurosporine exposure.
n: not reported in source
Cell lines or primary culturesSource sentences
In particular, eNAD reduced staurosporine-induced loss of mitochondrial membrane potential and ensuing caspase activation.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
In cells, SIRT1 inhibition or silencing abolished protection from staurosporine provided by exogenous NAD.
In plain wordsIn cells, SIRT1 inhibition or silencing abolished the protection from staurosporine provided by exogenous NAD.
n: not reported in source
Cell lines or primary culturesSource sentences
Of importance, pharmacological inhibition or silencing of the NAD-dependent enzyme SIRT1 abrogated the ability of eNAD to provide protection from staurosporine, having no effect on eNAD-dependent protection from C2-ceramide or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
In cells, SIRT1 inhibition or silencing did not affect protection from C2-ceramide provided by exogenous NAD.
In plain wordsIn cells, SIRT1 inhibition or silencing did not affect the protection from C2-ceramide provided by exogenous NAD.
n: not reported in source
Cell lines or primary culturesSource sentences
Of importance, pharmacological inhibition or silencing of the NAD-dependent enzyme SIRT1 abrogated the ability of eNAD to provide protection from staurosporine, having no effect on eNAD-dependent protection from C2-ceramide or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
In cells, SIRT1 inhibition or silencing did not affect NAD-dependent protection from N-methyl-N'-nitro-N-nitrosoguanidine.
In plain wordsIn cells, SIRT1 inhibition or silencing did not affect NAD-dependent protection from N-methyl-N'-nitro-N-nitrosoguanidine.
n: not reported in source
Cell lines or primary culturesSource sentences
Of importance, pharmacological inhibition or silencing of the NAD-dependent enzyme SIRT1 abrogated the ability of eNAD to provide protection from staurosporine, having no effect on eNAD-dependent protection from C2-ceramide or N-methyl-N'-nitro-N-nitrosoguanidine.
Here, we report that intracellular NAD contents increased upon exposure of cell lines or primary cultures to exogenous NAD (eNAD).
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
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