Foenumoside B isolated from Lysimachia foenum-graecum extract suppresses LPS-induced inflammatory response via NF-kappa B/AP-1 inactivation in murine macrophages and in endotoxin-induced shock model
- Authors
- Choi, Hye-Eun; Kwak, Hyun Jeong; Kim, Seul Ki; Cheon, Hyae Gyeong
- Issue Date
- 5-Aug-2018
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- FSB; LPS; Inflammation; Macrophage; Sepsis; NF-kappa B; AP-1
- Citation
- EUROPEAN JOURNAL OF PHARMACOLOGY, v.832, pp.120 - 128
- Journal Title
- EUROPEAN JOURNAL OF PHARMACOLOGY
- Volume
- 832
- Start Page
- 120
- End Page
- 128
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3464
- DOI
- 10.1016/j.ejphar.2018.05.022
- ISSN
- 0014-2999
- Abstract
- Foenumoside B (FSB), a bioactive component isolated from the Lysimachia foenum-graecum extract (LFE), has been shown to possess anti-inflammatory effects, but the underlying molecular mechanisms involved have not been elucidated. Accordingly, the authors investigated the mechanisms responsible for the anti-inflammatory effects of FSB in murine macrophages activated by LPS. FSB suppressed the LPS-induced expressions of iNOS and COX-2 at protein and mRNA levels and consequently decreased NO and PGE2 production in RAW264.7 and primary macrophages. FSB also reduced the LPS-induced inductions of TNF-alpha, IL-6 and IL-1 beta at protein and mRNA levels. Studies of the molecular mechanisms involved in the anti-inflammatory effects of FSB showed that it inhibited the transcriptional activities of NF-kappa B and AP-1, and the nuclear translocation of NF-kappa B via inhibition of the phosphorylations of AKT, p38 and STAT3. In a sepsis model, pretreatment with FSB inhibited the LPS-stimulated mRNA and protein levels of proinflammatory mediators, such as, iNOS, COX-2, TNF-alpha, IL-6 and IL-1 beta in plasma and liver. Importantly, FSB increased the survival rate of mice in the LPS-induced sepsis model. Taken together, these results show that the anti-inflammatory effects of FSB against LPS-induced inflammatory conditions are associated with inhibitions of the phosphorylations of AKT, p38 and STAT3 followed by the transcriptional suppressions of NF-kappa B and AP-1, and thus, reduced expressions of pro-inflammatory genes.
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