烟酰胺通过抑制 MAPK 和 NF-κB 信号通路减轻急性肺损伤的机制。
The mechanism of nicotinamide on reducing acute lung injury by inhibiting MAPK and NF-κB signal pathway.
机构信息
Department of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, No. 218, Ziqiang Street, Nanguan District, Changchun, 130000, Jilin, China.
Department of Respiration, General Hospital of Jilin Tonghua Mining Co., Ltd, No. 67, Nanling Street, Hunjiang District, Baishan, 134300, Jilin, China.
出版信息
Mol Med. 2021 Sep 20;27(1):115. doi: 10.1186/s10020-021-00376-2.
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-κB signaling pathways.
CONCLUSION
These results suggested that NAM may reduce the release of proinflammatory mediators by inhibiting the MAPK and AKT/NF-κB signaling pathways and ultimately alleviate lung injury.
背景
急性肺损伤是导致肺炎患者死亡的重要因素。既往研究表明烟酰胺（NAM）在减轻细胞损伤方面发挥作用，因此本研究探索了 NAM 在急性肺损伤中的作用机制。
方法
通过 qRT-PCR、western blot 和 ELISA 等方法，我们在体内和体外探索了 NAM 影响急性肺损伤的机制。
结果
结果表明，NAM 可显著减轻肺损伤和促炎介质的积累。进一步的机制研究表明，NAM 可显著抑制 MAPK 和 AKT/NF-κB 信号通路。
结论
这些结果表明，NAM 可能通过抑制 MAPK 和 AKT/NF-κB 信号通路减少促炎介质的释放，从而缓解肺损伤。
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