Basic Medical College, Qingdao University of Medicine, 38 Dengzhou Road, Qingdao 266021, PR China.
Food Funct. 2018 Feb 21;9(2):1214-1223. doi: 10.1039/c7fo01677h.
Recent research studies have shown that the intestinal flora are related to the occurrence and progress of breast cancer. This study investigates the effect of fucoidan on intestinal flora and intestinal barrier function in rats with 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast cancers. Sixty female Sprague-Dawley rats were randomly assigned to the control group, the model group, and the F1 and F2 groups, which were fed fucoidan at concentrations of 200 and 400 mg per kg bw (body weight), respectively. Intestinal histopathological analysis was performed and 16S rDNA high-throughput sequencing was used to provide an overview of the intestinal flora composition. The contents of d-lactic acid (d-LA), diamine oxidase (DAO) and endotoxin in plasma were detected by ELISA. Expression levels of the tight junction (TJ) proteins, phosphorylated p38 MAPK and ERK1/2 were measured using western blotting. Our results suggested that the intestinal wall of the model group was damaged. However, after fucoidan intervention, the villi were gradually restored. ELISA showed that the levels of plasma endotoxin, d-LA and DAO decreased in the F1 and F2 groups compared to those in the model group. Fucoidan treatment also increased the expressions of ZO-1, occludin, claudin-1 and claudin-8. Furthermore, the expression levels of phosphorylated p38 MAPK and ERK1/2 were upregulated in fucoidan treatment groups. The results of 16S rDNA high-throughput sequencing indicated that fucoidan increased the diversity of the intestinal microbiota and induced changes in microbial composition, with the increased Bacteroidetes/Firmicutes phylum ratio. In conclusion, the supplement of fucoidan could improve the fecal microbiota composition and repair the intestinal barrier function. The study suggested the use of fucoidan as an intestinal flora modulator for potential prevention of breast cancer.
最近的研究表明,肠道菌群与乳腺癌的发生和发展有关。本研究探讨了岩藻聚糖对 7,12-二甲基苯并[a]蒽(DMBA)诱导的乳腺癌大鼠肠道菌群和肠道屏障功能的影响。将 60 只雌性 Sprague-Dawley 大鼠随机分为对照组、模型组和 F1 组、F2 组,分别灌胃 200 和 400 mg/kg bw 的岩藻聚糖。进行肠道组织学分析,并采用 16S rDNA 高通量测序对肠道菌群组成进行概述。通过 ELISA 检测血浆中 d-乳酸(d-LA)、二胺氧化酶(DAO)和内毒素的含量。采用 Western blot 法检测紧密连接(TJ)蛋白、磷酸化 p38 MAPK 和 ERK1/2 的表达水平。结果表明,模型组的肠壁受损。然而,岩藻聚糖干预后,绒毛逐渐恢复。ELISA 结果显示,F1 组和 F2 组血浆内毒素、d-LA 和 DAO 水平均低于模型组。岩藻聚糖处理还增加了 ZO-1、occludin、claudin-1 和 claudin-8 的表达。此外,岩藻聚糖处理组磷酸化 p38 MAPK 和 ERK1/2 的表达水平上调。16S rDNA 高通量测序结果表明,岩藻聚糖增加了肠道微生物群的多样性,并诱导微生物组成发生变化,厚壁菌门/拟杆菌门比值增加。综上所述,岩藻聚糖的补充可以改善粪便微生物群组成并修复肠道屏障功能。该研究表明,岩藻聚糖作为一种肠道菌群调节剂,可用于预防乳腺癌。