Protective effects of nicotinamide mononucleotide against oxidative stress-induced PC12 cell death via mitochondrial enhancement

In this study, we hypothesized that NMN attenuates oxidative stress-induced cell damage via sirtuin activation and increased numbers of mitochondria. To investigate whether NMN can protect neuronal cells from oxidative stress via the enhancement of mitochondrial function, we used PC12 cells treated with 6-hydroxydopamine (6-OHDA) or hydrogen peroxide (H2O2) as oxidative stress models. With regard to cytoprotective effects, pretreatment with NMN significantly reduced cell death induced by these stressors. These protective effects were attenuated by the sirtuin inhibitor, sirtinol, and knock-down of the peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α), which activates mitochondrial biogenesis. To clarify if NMN increased mitochondria, intracellular mitochondria were quantified using cytometric analysis. NMN clearly increased the numbers of intracellular mitochondria, and this increase was attenuated by sirtinol. Moreover, we quantified the mitochondria-associated proteins Sirt3 and superoxide dismutase 2 (SOD2) and found that treatment with NMN increased these proteins. We conclude that NMN protects neuronal cells from oxidative stress via sirtuin activation followed by mitochondrial enhancement.Graphical abstract

Source: PharmaNutrition - December 8, 2019 Category: Nutrition Source Type: research