Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H O -induced damage via NAMPT and the NF-κB p65 signalling pathway.

An increasing number of studies have shown that nicotinamide mononucleotide (NMN) can inhibit not only ageing but also oxidative stress and inflammatory reactions by improving energy metabolism. However, the role of NMN in regulating the anti-apoptotic, antioxidative stress and inflammatory responses of brain microvascular endothelial cells is still unknown. Therefore, here we studied the effects of NMN on H O -induced oxidative damage of bEnd.3 cells. In this study, we found that NMN could inhibit the NF-κBp65 inflammatory signalling pathway and increase the expression of the enzymes NAMPT, VEGF and eNOS, alleviating H O -induced apoptosis in bEnd.3 cells. Taken together, these results suggest that NMN reduces H O -induced oxidative stress and apoptosis and improves cell functions by inhibiting the NF-κBp65 inflammatory pathway and increasing NAMPT expression.