Gancaonin N from Glycyrrhiza uralensis Attenuates the Inflammatory Response by Downregulating the NF-κB/MAPK Pathway on an Acute Pneumonia In Vitro Model

Acute pneumonia is an inflammatory disease caused by several pathogens, with symptoms such as fever and chest pain, to which children are particularly vulnerable. Gancaonin N is a prenylated isoflavone of Glycyrrhiza uralensis that has been used in the treatment of various diseases in oriental medicine. There are little data on the anti-inflammatory efficacy of Gancaonin N, and its effects and mechanisms on acute pneumonia are unknown. Therefore, this study was conducted as a preliminary analysis of the anti-inflammatory effect of Gancaonin N in lipopolysaccharide (LPS)-induced RAW264.7 cells, and to identify its preventive effect on the lung inflammatory response and the molecular mechanisms underlying it. In this study, Gancaonin N inhibited the production of NO and PGE2 in LPS-induced RAW264.7 cells and significantly reduced the expression of iNOS and COX-2 proteins at non-cytotoxic concentrations. In addition, in LPS-induced A549 cells, Gancaonin N significantly reduced the expression of COX-2 and pro-inflammatory cytokines, such as TNF-alpha, IL-1 beta, and IL-6. Moreover, Gancaonin N reduced MAPK signaling pathway phosphorylation and NF-kappa B nuclear translocation. Therefore, Gancaonin N relieved the inflammatory response by inactivating the MAPK and NF-kappa B signaling pathways; thus, it is a potential natural anti-inflammatory agent that can be used in the treatment of acute pneumonia.

Automated summary

This study demonstrated that Gancaonin N possesses anti-inflammatory effects by inhibiting the production of NO and PGE2, reducing the expression of iNOS and COX-2, and decreasing the levels of pro-inflammatory cytokines in LPS-induced cells. Furthermore, Gancaonin N suppressed the MAPK signaling pathway and NF-kappa B nuclear translocation, suggesting its potential as a natural anti-inflammatory agent for the treatment of acute pneumonia.