1. Academic Validation
  2. Secoisolariciresinol diglucoside suppresses Dextran sulfate sodium salt-induced colitis through inhibiting NLRP1 inflammasome

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

  • Int Immunopharmacol. 2020 Jan;78:105931. doi: 10.1016/j.intimp.2019.105931.
Zhen Wang 1 Tuo Chen 2 Chunrong Yang 3 Ting Bao 1 Xiaoli Yang 1 Fang He 4 Yanting Zhang 4 Lili Zhu 5 Hongbo Chen 6 Shikuo Rong 7 Shaoqi Yang 8
Affiliations

Affiliations

  • 1 Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia, China; College of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia, China.
  • 2 College of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia, China.
  • 3 Department of Gastroenterology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
  • 4 Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia, China.
  • 5 College of Basic Medicine, Ningxia Medical University School, Yinchuan, Ningxia, China.
  • 6 Department of Cardiology, First People's Hospital of Jining, Jining, Shandong, China.
  • 7 College of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia, China. Electronic address: [email protected].
  • 8 Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia, China; College of Clinical Medicine, Ningxia Medical University, Yinchuan 750004, Ningxia, China. Electronic address: [email protected].
Abstract

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

Keywords

Colitis; IL-18; IL-1β; NF-κB; NLRP1 inflammasome; RAW264.7 mouse macrophages; Secoisolariciresinol diglucoside; TNF-α.

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