Objective To investigate the role of nicotinamide mononucleotide (NMN) in D-galactose (D-gal) induced aging kidney in mice and its possible anti-inflammatory mechanism. Methods Twenty-four male C57BL/6 mice were randomly divided into control group, NMN group, D-gal group and D-gal+NMN group. The mouse model of renal aging was established by subcutaneous injection of D-gal. The body mass of each group was recorded. All mice were sacrificed and the kidneys were removed and sectioned for HE staining and Masson staining to observe pathological changes and detect the severity of renal interstitial fibrosis. Senescence-related β-galactosidase(SA-β-gal) staining was used to evaluate renal aging. Immunohistochemistry (IHC) staining and Western blot were employed to observe the distribution and abundance of p16 and p21 in the kidneys. The protein levels anti-aging gene silent information regulator 1 (SIRT1), and inflammatory indicators, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and nuclear factor-κB (NF-κB) in the kidneys were also detected by Western blot. Results NMN had no significant effect on body mass of the mice from the D-gal group (P>0.05). Compared with the control group, the D-gal group presented glomerular atrophy, tubule swelling and dilatation, and renal interstitial fibrosis, increased expression of p16 and p21, which mainly located in the renal tubules, as well as enhanced SA-β-gal activity (all P<0.05). Western blot showed that the expression levels of p16 and p21, and those of TNF-α, IL-1β and NF-κB were obviously up-regulated, while that of SIRT1 was decreased in the D-gal group (P<0.05). NMN treatment remarkably attenuated glomerular atrophy, tubule swelling and dilatation, and renal interstitial fibrosis, reduced the indicators related to aging and inflammation, and alleviated the down-regulation of SIRT1 and increase of SA-β-gal activity in the D-gal group (all P<0.05). Conclusion NMN may delay D-gal-induced renal aging by promoting SIRT1 expression and inhibiting NF-κB pathway mediated inflammatory response.