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    國內團隊:三氯蔗糖惡化小鼠的結腸炎相關結直腸癌

    發布日期:2021-03-11
      1.三氯蔗糖惡化AOM/DSS誘導的小鼠結腸炎相關結直腸癌,降低體重及結腸長度,增加結直腸腫瘤的數量/大小、結腸炎病理評分、脾臟重量及死亡率;

      2.三氯蔗糖促進AOM/DSS誘導的消化蛋白酶活性變化,進一步增加胰蛋白酶及糜蛋白酶活性,并降低β-葡萄糖醛酸酶的活性;

      3.三氯蔗糖惡化AOM/DSS誘導的腸道屏障功能損傷,并改變腸道菌群組成;

      4.三氯蔗糖增加結腸的炎癥因子(TNF-α、IL-1β)及TLR4/MyD88表達,降低IL-10表達,并上調STAT3-VEGF信號。

      主編推薦語

      三氯蔗糖是一種無熱量的人工甜味劑,被用于多種食品及飲料中。哈爾濱醫科大學附屬二院的姜明山團隊及哈爾濱醫科大學的王秀宏團隊在Frontiers in Oncology上發表的一項最新研究,在AOM/DSS誘導的結腸炎相關結直腸癌小鼠模型中,三氯蔗糖可促進腫瘤發生,并導致腸道菌群失調,破壞腸道屏障功能,降低消化蛋白酶活性,惡化結腸炎癥。


    Frontiers in Oncology
                      [IF:4.848]

    Sucralose Promotes Colitis-Associated Colorectal Cancer Risk in a Murine Model Along With Changes in Microbiota

    三氯蔗糖促進小鼠模型的結腸炎相關結直腸癌風險,并伴隨著菌群變化

    10.3389/fonc.2020.00710
    2020-06-03, Article

    Abstract:

    Sucralose is a calorie-free high-intensity artificial sweetener that is widely used in thousands of foods and beverages all over the world. Although it was initially regarded as a safe, inert food additive, its adverse effect on gut microbiota and health has drawn more and more attention as evidence accumulates. Studies by us and others revealed that sucralose exacerbated gut damage and inflammation in animal models for inflammatory bowel disease (IBD), including those for both ulcerative colitis, and Crohn's disease. Our study demonstrated that sucralose greatly aggravated dextran sulfate sodium (DSS)-induced colitis along with causing changes in gut microbiota, the gut barrier and impaired inactivation of digestive proteases mediated by deconjugated bilirubin. It is well-documented that IBD greatly increases the risk of colorectal cancer (CRC), the globally third-most-common cancer, which, like IBD, has a high rate in the developed countries. Azoxymethane (AOM)/DSS has been the most commonly used animal model for CRC. In this study, we further explored the effect of sucralose on tumorigenesis and the possible mechanism involved using the AOM/DSS mouse model. First, 1.5 mg/ml sucralose was included in the drinking water for 6 weeks to reach a relatively stable phase of impact on gut microbiota. Then, 10 mg/kg AOM was administered through intraperitoneal injection. Seven days later, 2.5% DSS was put in the drinking water for 5 days, followed by 2 weeks without DSS. The 5 days of DSS was then repeated, and the mice were sacrificed 6 weeks after AOM injection. The results showed that sucralose caused significant increases in the number and size of AOM/DSS-induced colorectal tumors along with changes in other parameters such as body and spleen weight, pathological scores, mortality, fecal β-glucuronidase and digestive proteases, gut barrier molecules, gut microbiota, inflammatory cytokines and pathways (TNFα, IL-1β, IL-6, IL-10, and TLR4/Myd88/NF-κB signaling), and STAT3/VEGF tumor-associated signaling pathway molecules. These results suggest that sucralose may increase tumorigenesis along with dysbiosis of gut microbiota, impaired inactivation of digestive protease, damage to the gut barrier, and exacerbated inflammation.
    First Authors:
    Xueting Li
    Correspondence Authors:
    Xiuhong Wang,Mingshan Jiang
    All Authors:
    Xueting Li,Yuanli Liu,Yan Wang,Xue Li,Xinran Liu,Mengru Guo,Yiwei Tan,Xiaofa Qin,Xiuhong Wang,Mingshan Jiang

      來源:網絡


     
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