NMN: a Novel Therapeutic Direction for Sepsis-induced Acute Lung Injury

NMN Administration: a Novel Therapeutic Direction for Sepsis-induced Acute Lung Injury



1. Introduction

Acute lung injury comprises a uniform response of the lung to inflammatory or chemical insults which is commonly caused by systemic illness including sepsis or trauma, infection with pathogens, and toxic gas inhalation. Sepsis-induced acute lung injury is a leading cause of morbidity and mortality worldwide, imposing substantial economic, social, and health burdens. Despite advances in knowledge of septic pulmonary pathologies over the years, efficient targeted therapies are still lacking. Notably, NMN administration has been uncovered to be effective in alleviating sepsis-induced acute lung injury, which can reduce cellular inflammation, oxidative stress, and apoptosis.

2. The impact of NMN upon macrophage polarization in LPS-induced MH-S cells 

In mouse alveolar macrophage cell line MH-S treated by lipopolysaccharide (LPS), NMN can facilitate the transformation of macrophages from pro-inflammatory M1 phenotype towards the anti-inflammatory M2 phenotype to promote inflammatory resolution and tissue repair, as evidenced by the downregulation of M1 phenotype-associated markers (iNOS and CD86+ F4/80+) and pro-inflammatory cytokines (IL-1β, TNF-α and IL-6) as well as the upregulation of M2 phenotype-related markers (Arg1 and CD86+ F4/80+) and anti-inflammatory mediators (IL-10) post NMN administration.

3. The alleviation of LPS-induced lung injury post NMN administration

In vitro, NMN represses the apoptosis and production of pro-inflammatory factors in LPS-stimulated MH-S cells. In vivo, NMN explicitly ameliorates LPS-induced pathological alterations, encompassing thickened alveolar wall, inflammatory cell infiltration, septa swelling, and erythrocyte exudation, in a murine septic model.

4. The association of SIRT1/NF-κB signaling activation with NMN-mediated macrophage polarization

SIRT1/NF-κB signaling pathway is involved in the lung protection of NMN, as manifested by the elevated expression of SIRT1 as well as the reduced acetylation and phosphorylation of NF-κB-p65 post NMN treatment.



Repression of SIRT1/NF-κB signaling offsets NMN-mediated M2 macrophage polarization. SIRT1 inhibitor EX-527 decreases the expression of SIRT1, yet increases the expression of acetylated and phosphorylated NF-κB-p65 in septic mice pretreated with NMN. In contrast to NMN, EX-527 overtly promotes the expression levels of M1 macrophage-associated markers (iNOS and CD86) while inhibiting those of M2 phenotype-related markers (Arg1 and CD206). 

5. Conclusion

NMN can effectively ameliorate LPS-induced acute lung injury through modulating macrophage polarization via SIRT1/NF-κB signalling pathway, providing a novel therapeutic direction for sepsis-induced acute lung injury.

6. Reference

He, Simeng et al. “Nicotinamide mononucleotide alleviates endotoxin-induced acute lung injury by modulating macrophage polarization via the SIRT1/NF-κB pathway.” Pharmaceutical biology vol. 62,1 (2024): 22-32. doi:10.1080/13880209.2023.2292256

BONTAC NMN



BONTAC is the leader of the global NMN industry, with the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 160 invention patents including 15 NMN patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. Both the high-quality product and excellent service can be better ensured in BONTA. BONTAC has 12 years of industry experience, which is worthy of your trust.

Disclaimer

This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. 


 

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