Angelicin regulates LPS-induced inflammation via inhibiting MAPK/NF-kappa B pathways

作者:Liu, Fang; Sun, Guo-quan; Gao, Hua-yi; Li, Rui-sheng; Soromou, Lanan-Wassy; Chen, Na; Deng, Yan-Hong; Feng, Hai-hua*
来源:Journal of Surgical Research, 2013, 185(1): 300-309.
DOI:10.1016/j.jss.2013.05.083

摘要

Background: Angelicin is a furocoumarin found in Psoralea corylifolia L. fruit. The purpose of this study was to investigate the protective ability of angelicin against inflammation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and LPS-induced in vivo acute lung injury model. Materials and methods: The concentrations of tumor necrosis factor alpha (TNF-alpha) and interleukin (IL)-6 in the culture supernatants of RAW 264.7 cells were determined 24 h after LPS administration. ALI was induced by intratracheal instillation of LPS. Six hours after LPS inhalation, bronchoalveolar lavage fluid and lung tissue samples were obtained for enzyme-linked immunosorbent assay, histologic, and Western blotting analyses. Results: The results showed that pretreatment with angelicin markedly downregulated TNF-alpha and IL-6 levels in vitro and in vivo, and significantly decreased the amount of inflammatory cells, lung wet-to-dry weight ratio, and myeloperoxidase activity in LPS-induced ALI mice. Furthermore, Western blotting analysis results demonstrated that angelicin blocked the phosphorylation of I kappa B alpha, NF-kappa Bp65, p38 MAPK, and JNK in LPS-induced ALI. Conclusions: These results suggest that angelicin was potentially advantageous to prevent inflammatory diseases by inhibiting NF-kappa B and MAPK pathways. Our data indicated that angelicin might be a potential new agent for prevention of inflammatory reactions and diseases in the clinic.