Nicotinamide adenine dinucleotide (
NAD(+)) plays critical roles in energy metabolism, mitochondrial functions,
calcium homeostasis and immunological functions. Our previous studies have found that
NAD(+) administration can profoundly decrease ischemic
brain injury and
traumatic brain injury. Our recent study has also provided first direct evidence indicating that
NAD(+) treatment can decrease cellular apoptosis, while the mechanisms underlying this protective effect remain unclear. In our current study, we determined the effects of
NAD(+) treatment on several major factors in apoptosis and
necrosis, including levels of Bax and nuclear translocation of
apoptosis-inducing factor (AIF), as well as levels of
DNA double-strand breaks (DSBs) and intracellular
ATP in
rotenone-treated differentiated PC12 cells. We found that
NAD(+) treatment can markedly attenuate the
rotenone-induced increases in the levels of Bax and nuclear translocation of AIF in the cells. We further found that
NAD(+) treatment can significantly attenuate the
rotenone-induced increase in the levels of DSBs and decrease in the intracellular
ATP levels. Collectively, our study has suggested mechanisms underlying the preventive effects of
NAD(+) on apoptosis, which has highlighted the therapeutic potential of
NAD(+) for decreasing apoptotic changes in multiple major diseases.