ReferenceID 1230
Asperuloside suppressing oxidative stress and inflammation in DSS-induced chronic colitis and RAW 264.7 macrophages via Nrf2/HO-1 and NF-κB pathways
Chem Biol Interact
BACKGROUND: Inflammatory bowel diseases (IBDs), which mainly include Crohn's disease (CD) and ulcerative colitis (UC), are chronic idiopathic inflammatory disease of the gastrointestinal tract for which effective pharmac
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Record Fields
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- Reference Id
- 1230
- Evidence Id
- 17820
- Core Evidence Id
- 17820
- Source Reference Id
- 2448
- Herb2 Reference Id
- HBREF003245
- Subject Paper Key
- HBIN017136_33974900
- Pubmed Id
- 33974900
- Doi
- 10.1016/j.cbi.2021.109512
- Paper Title
- Asperuloside suppressing oxidative stress and inflammation in DSS-induced chronic colitis and RAW 264.7 macrophages via Nrf2/HO-1 and NF-κB pathways
- Paper Abstract
- BACKGROUND: Inflammatory bowel diseases (IBDs), which mainly include Crohn's disease (CD) and ulcerative colitis (UC), are chronic idiopathic inflammatory disease of the gastrointestinal tract for which effective pharmacological treatments are lacking or options are very limited. PURPOSE: Here, we aim to investigate the therapeutic effects of an iridoid glycoside, asperuloside (ASP) on mice experimental chronic colitis induced by dextran sulfate sodium (DSS) and further explore underlying mechanisms in vitro and in vivo. METHODS: LPS-treated RAW 264.7 cells showed inflammation and were assessed for various physiological, morphological and biochemical parameters in the absence or presence of ASP. Chronic colitis was induced by 2% DSS in mice, which were used as an animal model to explore the pharmacodynamics of ASP. We detected p65 and Nrf2 pathway proteins via Western blot and RT-PCR analysis, assessed the cytokines TNF-alpha and IL-6 via ELISA, tested p65 and Nrf2 nuclear translocation via fluorescence. In addition, the docking affinity of ASP and p65 or Nrf2 proteins in the MOE 2015 software. RESULTS: We found that ASP attenuated weight loss, disease activity index (DAI) and colonic pathological damage in colitis mice and restored the expressions of inflammatory cytokines in the colon. In addition, ASP restored antioxidant capacity in DSS-induced chronic colitis mice and lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Furthermore, ASP suppressed oxidative stress through increasing Nrf2, HO-1 and NQO-1 proteins expressions, and down-regulated nuclear levels of p65 to inhibit DSS-induced colonic oxidative stress and inflammation. Validation of the molecular docking results also indicated that ASP interacts with Nrf2 or p65 proteins. In summary, ASP improved DSS-induced chronic colitis by alleviating inflammation and oxidative stress, activating Nrf2/HO-1 signaling and limiting NF-kappaB signaling pathway, which may be an effective candidate for the treatment of IBD.
- Journal
- Chem Biol Interact
- Publish Year
- 2021
- Experiment Subject
- mouse; lipopolysaccharide (lps)-stimulated raw 264.7 cells; raw 264.7 cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- Ulcerative Colitis; Chronic Idiopathic Inflammatory Disease Of The Gastrointestinal Tract; Inflammation; Crohn's Disease; Chronic Colitis; Ibds; Colitis; Inflammatory Bowel Diseases
- Paper Title Cn
- Paper Title En
- Asperuloside suppressing oxidative stress and inflammation in DSS-induced chronic colitis and RAW 264.7 macrophages via Nrf2/HO-1 and NF-κB pathways
- Bilingual Status
- semi_complete