ReferenceID 161
Stauntoside B inhibits macrophage activation by inhibiting NF-κB and ERK MAPK signalling
Pharmacol Res
Inflammation is a defensive reaction of body to resist foreign invasion. However, it has been demonstrated that excessive and continuous inflammatory responses contribute to various inflammatory diseases, including rheum
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Record Fields
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- Reference Id
- 161
- Evidence Id
- 16751
- Core Evidence Id
- 16751
- Source Reference Id
- 291
- Herb2 Reference Id
- HBREF000545
- Subject Paper Key
- HBIN044724_27343699
- Pubmed Id
- 27343699
- Doi
- 10.1016/j.phrs.2016.06.022
- Paper Title
- Stauntoside B inhibits macrophage activation by inhibiting NF-κB and ERK MAPK signalling
- Paper Abstract
- Inflammation is a defensive reaction of body to resist foreign invasion. However, it has been demonstrated that excessive and continuous inflammatory responses contribute to various inflammatory diseases, including rheumatoid arthritis. Nuclear factor-κB (NF-κB) regulates the expression of an array of inflammatory mediators, cytokines and chemokine genes in activated macrophages. Therefore, NF-κB has become an attractive drug target for controlling inflammation. In this study, stauntoside B, a C21 steroidal glycosides compound isolated from a Chinese medicine Cynanchi Stauntonii, was for the first time found to suppress macrophage activation induced by lipopolysaccharide (LPS) in RAW264.7 cells and rat primary peritoneal macrophages and could be a potent NF-κB inhibitor. The results showed that stauntoside B significantly reduced the release of inflammatory mediators in activated RAW264.7 cells and rat peritoneal macrophages, including nitric oxide (NO) and prostaglandin E2 (PGE2). The mRNA expressions of pro-inflammatory mediators and cytokines, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), microsomal prostaglandin synthetase-1 (mPGES-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) as well as the production of TNF-α and IL-6 were also inhibited by stauntoside B. Mechanistic investigation implies that the anti-inflammatory activity of stauntoside B could result from the suppression of LPS-induced IKKα/β activation, IκBα phosphorylation, p65 (ser536) NF-κB phosphorylation, and ERK MAPK activation by stauntoside B treatment in activated macrophages. Meanwhile, stauntoside B could induce apoptosis in LPS-activated macrophages. The current study suggests stauntoside B being a valuable candidate drug for the treatment of inflammatory diseases, especially for NF-κB activation associated inflammatory diseases.
- Journal
- Pharmacol Res
- Publish Year
- 2016
- Experiment Subject
- cells: lipopolysaccharide (lps) in raw264.7 cells and rat primary peritoneal macrophages
- Experiment Type
- Cell Experiment
- Phenotype Related
- Paper Title Cn
- Paper Title En
- Stauntoside B inhibits macrophage activation by inhibiting NF-κB and ERK MAPK signalling
- Bilingual Status
- semi_complete