The Journal of surgical researchNov 8, 2022

Nicotinamide Mononucleotide Reduces Lung Injury Caused by LPS Through Anti-Inflammatory, Antioxidant, and Cell-Protection Effects

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Feb 20, 2026

Abstract

Nicotinamide mononucleotide (NMN) significantly improved lung health in a mouse model of acute lung injury induced by lipopolysaccharide.

NMN treatment reduced pathological damage and cell death in lung tissue compared to the LPS group.
Levels of inflammatory cytokines TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid were decreased with NMN administration.
The total cell count and neutrophil count in bronchoalveolar lavage fluid were lower in the NMN-treated group.
NMN lowered the dry-to-wet ratio and malondialdehyde (MDA) content, indicators of lung injury.
Phosphorylation levels of p38 MAPK and p65 NF-κB were reduced with NMN treatment, suggesting decreased inflammation.
Superoxide dismutase (SOD) activity was increased following NMN treatment, indicating enhanced antioxidative response.

Simplified

INTRODUCTION: Nicotinamide mononucleotide (NMN) is a nucleotide that is commonly recognized for its role as an intermediate of nicotinamide adenine dinucleotide (NAD) biosynthesis with multiple pharmacological effects. The purpose of this study was to evaluate the protective effect of nicotinamide mononucleotide (NMN) against lipopolysaccharide (LPS)-induced acute lung injury (ALI). +

METHODS: We investigated the effect of NMN on ALI-induced inflammatory response, oxidative stress, and cell apoptosis. The ALI mouse model was performed by injecting LPS intratracheally at a dose of 10 mg/kg in 50 μL saline. Flow cytometry was used to detect neutrophil infiltration in bronchoalveolar lavage fluid (BALF), and ELISA was used to detect the contents of inflammatory cytokines TNF-α, IL-1β and IL-6 in BALF. Oxidative stress was evaluated by determining the superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in lung tissue. ROS formation was analyzed by immunofluorescence. Western blotting was performed to detect apoptotic levels and p38MAPK/NF-κB phosphorylation levels in lung tissue.

RESULTS: In the ALI mouse model, NMN showed a significant therapeutic effect compared to the LPS group. NMN attenuated the pathological damage and cell apoptosis in lung tissue, decreased the levels of TNF-α, IL-1β, and IL-6 in BALF, and reduced the number of total cells and neutrophils in BALF. In addition, NMN attenuated the LPS-induced elevation of dry-to-wet ratio, MDA content, p38 MAPK and p65 NF-κB phosphorylation levels, and the SOD activity was increased by NMN treatment.

CONCLUSIONS: In conclusion, the present study showed that NMN exerted a protective effect on LPS-induced ALI with anti-inflammatory, antioxidative, and antiapoptotic effects.

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Nicotinamide Mononucleotide Reduces Lung Injury Caused by LPS Through Anti-Inflammatory, Antioxidant, and Cell-Protection Effects

Abstract

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