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国内团队:三氯蔗糖恶化小鼠的结肠炎相关结直肠癌

时间:2021-03-11 08:09来源:热心肠日报 作者:szx 浏览次数:
  1.三氯蔗糖恶化AOM/DSS诱导的小鼠结肠炎相关结直肠癌,降低体重及结肠长度,增加结直肠肿瘤的数量/大小、结肠炎病理评分、脾脏重量及死亡率;

  2.三氯蔗糖促进AOM/DSS诱导的消化蛋白酶活性变化,进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;

  3.三氯蔗糖恶化AOM/DSS诱导的肠道屏障功能损伤,并改变肠道菌群组成;

  4.三氯蔗糖增加结肠的炎症因子(TNF-α、IL-1β)及TLR4/MyD88表达,降低IL-10表达,并上调STAT3-VEGF信号。

  主编推荐语

  三氯蔗糖是一种无热量的人工甜味剂,被用于多种食品及饮料中。哈尔滨医科大学附属二院的姜明山团队及哈尔滨医科大学的王秀宏团队在Frontiers in Oncology上发表的一项最新研究,在AOM/DSS诱导的结肠炎相关结直肠癌小鼠模型中,三氯蔗糖可促进肿瘤发生,并导致肠道菌群失调,破坏肠道屏障功能,降低消化蛋白酶活性,恶化结肠炎症。


Frontiers in Oncology
                  [IF:4.848]

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

三氯蔗糖促进小鼠模型的结肠炎相关结直肠癌风险,并伴随着菌群变化

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





 
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