Secoisolariciresinol diglucoside suppresses Dextran sulfate sodium salt-induced colitis through inhibiting NLRP1 inflammasome

• DOI: 10.1016/j.intimp.2019.105931
• Publication Date: 2019-12-05T01:55:56Z
• Authors: Zhen Wang; Tuo Chen; Chunrong Yang; Ting Bao; Xiaoli Yang; Fang He; Yanting Zhang; Lili Zhu; Hongbo Chen; Shikuo Rong; Shaoqi Yang
• Keywords: Lipopolysaccharides; Male; 0301 basic medicine; Colon; Inflammasomes; Dextran Sulfate; Anti-Inflammatory Agents; Colitis; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; RAW 264.7 Cells; Glucosides; Animals; Cytokines; Apoptosis Regulatory Proteins; Butylene Glycols; Adaptor Proteins, Signal Transducing

Inflammatory bowel disease (IBD) is a chronic and recurrent intestinal inflammatory with high risks for colorectal cancer extremely affect people's health. Secoisolariciresinol diglucoside (SDG), major component of lignans, exerts anti-inflammatory effects against digestive system diseases through multi-target mechanism. However, the effect SDG on IBD not clear. In present study, we aimed to investigate elucidate underlying The Dextran Sulfate Sodium Salt (DSS)-induced colitis model lipopolysaccharide (LPS) stimulated RAW264.7 mouse macrophages cellular inflammation were established. Morphological pathological changes in tissue mice observed by HE staining. Macrophage infiltration was detected flow cytometry. levels nucleotide oligomerization domain-like receptor protein 1 (NLRP1) inflammasome complexes, nuclear factor-kappa B (NF-κB) cytokines determined using quantitative real-time polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay. results showed that significantly attenuated severity number macrophage mice. Besides, decreased (IL-1β, IL-18 TNF-α) inhibited activation NLRP1 DSS-induced macrophages. Moreover, inhibitory partly dependent disruption NF-κB activation. Our indicated relieves inhibiting inflammasome, Therefore, may be potential treatment option IBD.