18β-glycyrrhetinic Acid Protects against Staphylococcus aureus Infection by Regulating the NF-κB Pathway

Background: 18 beta-glycyrrhetinic acid (18 beta-GA) is reported to possess various pharmacological properties of which anti-inflammatory activities has been widely explored. However, the role of 18 beta-GA in Staphylococcus aureus (SA) infection has not been investigated. The aim of the present study was to explore the effects of 18 beta-GA on the SA infection especially the SA-induced Acute lung injury (ALI) and its related mechanisms. Material and methods: We infected the mice or cells with SA and then detected the survival rates of mice, bacterial burden and production of proinflammatory cytokines both in vitro and in vivo. We then detected the High-mobility group box 1 (HMGB1) expression by RT-qPCR and Western blotting. The effects on NF-kappa B activation was also determined by Western blotting and luciferase assay. Results: 18 beta-GA could significantly improve the survival rate of SA-infected mice, reduce bacterial burden, suppress infiltration of inflammatory cells and reduce secretion of IL-1 beta, IL-6 and TNF-alpha both in lung tissues and cells. 18 beta-GA treatment decreased high-mobility group box 1 (HMGB1) expression induced by SA infection and neutralizing of HMGB1 could improve the survival rate of mice induced by SA, implying that 18 beta-GA protected SA infection through down-regulating HMGB1 expression. Finally, we demonstrated that 18 beta-GA inhibited the NF-kappa B activation. Conclusion: Taken together, our preliminary study suggested that 18 beta-GA provided protective effects against SA infection via its anti-inflammatory properties possibly through down-regulating the HMGB1/NF-kappa B activation.