The mechanism of nicotinamide on reducing acute lung injury by inhibiting MAPK and NF-κB signal pathway

Background Acute lung injury is an important factor that leads to the death of patients with pneumonia. Previous studies have shown that nicotinamide (NAM) plays a role in reducing cell damage, so this study explored the mechanism by which NAM functions in acute lung injury. Methods We explored the mechanism by which NAM affects acute lung injury in vivo and in vitro by qRT-PCR, western blotting and ELISA. Results The results showed that NAM could significantly reduce lung injury and proinflammatory mediator accumulation. Further mechanistic studies showed that NAM could significantly inhibit the MAPK and AKT/NF-kappa B signaling pathways. Conclusion These results suggested that NAM may reduce the release of proinflammatory mediators by inhibiting the MAPK and AKT/NF-kappa B signaling pathways and ultimately alleviate lung injury.

Automated summary

The study found that nicotinamide (NAM) can reduce proinflammatory mediator release in acute lung injury by inhibiting the MAPK and AKT/NF-kappa B signaling pathways, ultimately alleviating lung injury.