Abstract
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.
Keywords
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Article info
Publication history
Published online: November 05, 2022
Accepted:
September 18,
2022
Received in revised form:
August 23,
2022
Received:
February 22,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.