Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation
| Autor: | Gang Song, Shaoping Hu, Bing Zhang, Jiahui Yuan, Weiwei Wang, Tianhui Hu, Wei Zhong, Juan Li |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Mouse
Berberine Metabolite medicine.medical_treatment Cancer Treatment lcsh:Medicine Pharmacology Biochemistry Inflammatory bowel disease Mice chemistry.chemical_compound Drug Discovery Gastrointestinal Cancers Medicine lcsh:Science Multidisciplinary biology Anti-Inflammatory Agents Non-Steroidal Dextran Sulfate NF-kappa B Animal Models Colitis Cytokine Oncology Myeloperoxidase Cytokines Inflammation Mediators medicine.symptom Immunohistochemical Analysis Research Article Signal Transduction Drugs and Devices Drug Research and Development Colon Immunology Inflammation Gastroenterology and Hepatology Cell Line Rectal Cancer Model Organisms Complementary and Alternative Medicine Gastrointestinal Tumors Ulcerative Colitis Animals Biology Peroxidase business.industry Macrophages lcsh:R Inflammatory Bowel Disease Immunity Cancers and Neoplasms medicine.disease NFKB1 Disease Models Animal IκBα chemistry Immune System Immunologic Techniques biology.protein lcsh:Q Clinical Immunology business |
| Zdroj: | PLoS ONE PLoS ONE, Vol 9, Iss 2, p e87810 (2014) |
| ISSN: | 1932-6203 |
| Popis: | Phytogenic compounds with anti-oxidant and anti-inflammatory properties, such as ginsenoside metabolite compound K (CK) or berberine (BBR), are currently discussed as promising complementary agents in the prevention and treatment of cancer and inflammation. The latest study showed that ginsenoside Rb1 and its metabolites could inhibit TNBS-induced colitis injury. However, the functional mechanisms of anti-inflammation effects of ginsenoside, particularly its metabolite CK are still not clear. Here, using dextran sulfate sodium (DSS)-induced colitis in mice, clinical parameters, intestinal integrity, pro-inflammatory cytokines production, and signaling pathways in colonic tissues were determined. In mild and sever colitis mice, CK and BBR (as a positive agent) alleviated colitis histopathology injury, ameliorated myeloperoxidase (MPO) activity, reduced pro-inflammatory cytokines production, such as, IL-6, IL-1β, TNF-α, and increased anti-inflammatory cytokine IL-10 production in both mice colon tissues and blood. Nevertheless, the results revealed that CK and BBR inhibited NF-κB p65 nuclear translocation, downregulated p-IκBα and upregulated IκBα, indicating that CK, as well as BBR, suppressed the activation of the NF-κB pathway in the progression of colitis with immunofluorescence, immunohistochemical and western blotting analysis. Furthermore, CK inhibited pro-inflammatory cytokines production in LPS-activated macrophages via down-regulation of NF-κB signaling pathway. Taken together, our results not only reveal that CK promotes the recovery of the progression of colitis and inhibits the inflammatory responses by suppressing NF-κB activation, but also suggest that CK downregulates intestinal inflammation through regulating the activation of macrophages and pro-inflammatory cytokines production. |
| Databáze: | OpenAIRE |
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