NMN, also known as nicotinamide mononucleotide, is a ribo-nucleotide that is involved in nicotinamide phosphoribosyl-transferase (NAPRT) activity. It is a key intermediate in the salvage synthesis of NAD+. It is a precursor of nicotinic acid mononucleotide. NMN is also an inhibitor of NAMPT.

Nicotinamide riboside (NR) is synthesized by NAPRT and nicotinamide mononucleotide adenylyltransferase (NMAT). NAM is metabolized to NMN by NAMPT. This is the rate-limiting step of the salvage pathway. In DN, a lack of NR can impair NAD+ anabolism and fibrosis. It is therefore necessary to replenish the NAD+ pool.

This study was conducted to investigate the relationship between NMN and the NF-kB P65/FN signaling pathway in MSC. It was found that NMN was able to reduce the expression of Sirt1 in MSC. Interestingly, this protein plays an important role in DN pathogenesis.

In order to examine the effect of NMN on FN expression, a western blot was performed to measure FN, NMNAT1, and NAPRT expression. The expression of NAM, NMN, and NAMPT decreased, but the FN level increased with NAMPT overexpression. In addition, ROS levels were higher in the overexpressed group. These results suggest that NF-kB P65 and NMN are related to each other.

NMN inhibits the cytoplasmic exchange of mitochondria and aggravates inflammation. Furthermore, axonal denaturation is promoted by NMN. Its inhibition may be a new therapeutic target for the treatment of DN. It can promote the synthesis of nitric oxide. However, more research is needed to determine whether NMN is safe during pregnancy or breast-feeding.