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Published on: February 27, 2014
Therapeutic effects of lentinan on inflammatory bowel disease and colitis-associated cancer
Yanrong Liu1,2, Jianmin Zhao3, Yali Zhao1,4
1Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China.
Abstract:
In this study, we investigated the therapeutic potential of lentinan in mouse models of inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Lentinan decreased the disease activity index and macroscopic and microscopic colon tissue damage in dextran sulphate sodium (DSS)-induced or TNBS-induced models of colitis. High-dose lentinan was more effective than salicylazosulfapyridine in the mouse models of colitis. Lentinan decreased the number of tumours, inflammatory cell infiltration, atypical hyperplasia and nuclear atypia in azoxymethane/DSS-induced CAC model. It also decreased the expression of pro-inflammatory cytokines, such as IL-13 and CD30L, in IBD and CAC model mice possibly by inhibiting Toll-like receptor 4 (TLR4)/NF-κB signalling and the expression of colon cancer markers, such as carcinoembryonic antigen, cytokeratin 8, CK18 and p53, in CAC model mice. In addition, lentinan restored the intestinal bacterial microbiotal community structure in IBD model mice. Thus, it shows therapeutic potential in IBD and CAC model mice possibly by inhibiting TLR4/NF-κB signalling-mediated inflammatory responses and disruption of the intestinal microbiotal structure.
Insights
Lentinan shows therapeutic potential for inflammatory bowel disease (IBD) and colitis-associated cancer (CAC) in mouse models. It reduced inflammation, tissue damage, and tumor development by modulating key signaling pathways and gut microbiota.
Area of Science:
- Immunology
- Gastroenterology
- Pharmacology
Background:
- Inflammatory bowel disease (IBD) and colitis-associated cancer (CAC) are significant health concerns with limited therapeutic options.
- Current treatments for IBD and CAC have potential side effects and varying efficacy.
- Understanding the molecular mechanisms underlying IBD and CAC is crucial for developing novel therapies.
Purpose of the Study:
- To investigate the therapeutic efficacy of lentinan in preclinical models of IBD and CAC.
- To elucidate the potential mechanisms of action of lentinan in mitigating IBD and CAC.
- To evaluate lentinan's impact on inflammatory pathways, cancer markers, and gut microbiota.
Main Methods:
- Murine models of colitis (DSS-induced, TNBS-induced) and CAC (azoxymethane/DSS-induced) were utilized.
- Lentinan treatment was administered and compared with a standard drug, salicylazosulfapyridine.
- Disease activity, tissue damage, tumor burden, inflammatory cytokine expression (IL-13, CD30L), signaling pathways (TLR4/NF-κB), colon cancer markers, and gut microbiota composition were assessed.
Main Results:
- Lentinan significantly reduced disease activity index and colon tissue damage in colitis models.
- High-dose lentinan demonstrated superior efficacy compared to salicylazosulfapyridine in colitis models.
- Lentinan decreased tumor incidence, inflammatory cell infiltration, and atypical hyperplasia in the CAC model.
- Lentinan suppressed pro-inflammatory cytokine expression and colon cancer markers by inhibiting TLR4/NF-κB signaling.
- Lentinan treatment restored the intestinal bacterial community structure in IBD model mice.
Conclusions:
- Lentinan exhibits significant therapeutic potential for treating IBD and CAC in preclinical settings.
- Lentinan's efficacy is attributed to the inhibition of TLR4/NF-κB signaling, reducing inflammation and cancer progression.
- Lentinan also positively modulates the gut microbiota, contributing to its therapeutic effects in IBD.
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