β-Nicotinamide mononucleotide alleviates Alcohol-Induced liver injury in a mouse model through activation of NAD⁺/SIRT1 signaling pathways.

ABSTRACT:

Background

Alcoholism is a significant contributor to the development of alcoholic liver disease, for which no universally accepted and effective treatment currently exists. A precursor of NAD⁺, β-Nicotinamide mononucleotide (NMN), has revealed potential therapeutic benefits. However, its effectiveness in preventing ethanol-induced liver damage remains uncertain.

Methods

The objective of this study was to assess the protective effects of NMN and elucidate its potential mechanisms using a mouse model subjected to chronic and binge ethanol feeding. Eight-week-old C57BL/6J mice were randomly assigned to one of four groups (n = 10 per group): control (CTRL), ethanol (EtOH), ethanol with low-dose NMN (EtOH + NMN(L)), and ethanol with high-dose NMN (EtOH + NMN(H)). Foll

SUBMITTER: Yang X 

PROVIDER: S-EPMC12357478 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature