Abstract
Schisandra Fructus (SF) is a traditional Chinese herb used in the treatment of inflammatory disorders like hepatitis. One of the main anti-inflammatory components of SF is the lignans. However, the underlying anti-inflammatory mechanism of Schisandra Chinensis lignans (SCL) remains unclear. This study aims to investigate the effects of SCL on inflammatory mediators in lipopolysaccharide-stimulated RAW264.7 cells and explore the underlying mechanism. The production of nitric oxide (NO) was determined by Griess reaction. ELISA was used to determine cytokine levels and chemokines secretion. To estimate protein levels and enzyme activities, we employed Western blotting. Nuclear localization of NF-κB, AP-1, and IRF3 was detected using immunofluorescence analyses. The results showed that SCL significantly reduced the release of inflammatory mediators, including NO and PGE2, which may be related to down-regulation of iNOS and COX-2 expression. The production of cytokines and chemokines was suppressed by SCL treatment. SCL also decreased the phosphorylation of IKKα/β, IκB-α, Akt, TBK1, ERK, p38, JNK, NF-κB (p65), AP-1 (c-Jun), and IRF3 in RAW264.7 macrophages activated with LPS. The nuclear protein levels and nuclear translocation of AP-1, NF-κB and IRF3 were suppressed by SCL. These results indicated that SCL suppressed the IKKα/β/NF-κB, MAPKs/AP-1 and TBK1/IRF3 signaling pathways in LPS-stimulated RAW264.7 macrophages.
Highlights
Inflammation is a defensive response that evolved in higher organisms to protect them from infection and injury [1]
Schisandra Chinensis lignans (SCL) treatment obviously inhibited the expression of inducible nitric oxide synthase (iNOS) and COX-2 in LPS-stimulated RAW264.7 macrophages in a concentration dependent manner. These results suggested that the suppressive effect of SCL on nitric oxide (NO) and Prostaglandin E2 (PGE2) production is the result of the inhibition of iNOS and COX-2 expression, respectively
Our results showed that SCL effectively prevent the nuclear translocation of nuclear factor-κB (NF-κB) (p65), activator protein-1 (AP-1) (c-Jun), and interferon regulatory factor 3 (IRF3) in LPS-stimulated RAW264.7 cells
Summary
Inflammation is a defensive response that evolved in higher organisms to protect them from infection and injury [1]. Macrophages can be stimulated by various harmful stimuli, like lipopolysaccharide (LPS), an endotoxin that can initiate toll-like receptor (TLR)-4 signaling pathways, which activate transcription factors like nuclear factor-κB (NF-κB), activator protein-1 (AP-1) and interferon regulatory factor 3 (IRF3), leading to the release of pro-inflammatory cytokines and chemokines [9]. Overproduction of these inflammatory mediators will further activate immune cells and result in tissue damage and hemodynamic changes, organ failure, and death [10,11]. The TLR4 signaling pathway is one of the targets in treating inflammatory diseases
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
