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Galactooligosaccharide or 2′-Fucosyllactose Modulates Gut Microbiota and Inhibits LPS/TLR4/NF-κB Signaling Pathway to Prevent DSS-Induced Colitis Aggravated by a High-Fructose Diet in Mice
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2023-06-08 , DOI: 10.1021/acs.jafc.2c08814
Tao Chen 1 , Chuqing Wang 1 , Chenxi Nie 1 , Xiaojin Yuan 1 , Aobai Tu 1 , Juxiu Li 1
Affiliation  

A high-fructose diet (HFrD) has been reported to exacerbate dextran sulfate sodium (DSS)-induced colitis. 2′-Fucosyllactose (FL) and galactooligosaccharide (GOS) have been shown, respectively, to have preventive and ameliorative effects on colitis, while limited research has explored whether GOS and FL may be equally protective or preventive in mice with HFrD. Here, we evaluated the protective effects of FL and GOS on colitis exacerbated by feeding HFrD and explored the underlying mechanisms. DSS-induced colitis was studied in four randomized C57BL/6J male mice (n = 8 mice/group). Among them, three groups were fed with HFrD, and two received either GOS or FL treatment, respectively. Gut microbial composition was analyzed by 16S rDNA gene sequencing. Intestinal barrier integrity and inflammatory pathway expression were measured using qPCR, immunofluorescence, and Western blot methods. Compared to the HFrD group, GOS or FL treatment increased the α-diversity of the gut microbiota, reduced the relative abundance of Akkermansia, and increased the content of short-chain fatty acids (SCFAs), respectively. Compared with the HFrD group, GOS or FL treatment improved the loss of goblet cells and the reduction of tight junction protein expression, thereby improving intestinal barrier integrity. Also, GOS or FL inhibited the LPS/TLR4/NF-κB signaling pathway and oxidative stress to suppress the inflammatory cascade compared with the HFrD group. These findings suggest that GOS or FL intake can alleviate HFrD-exacerbated colitis, with no significant difference observed between GOS and FL treatments.

中文翻译:

低聚半乳糖或 2'-岩藻糖基乳糖调节肠道微生物群并抑制 LPS/TLR4/NF-κB 信号通路,以预防高果糖饮食加重 DSS 诱导的结肠炎

据报道,高果糖饮食(HFrD)会加剧葡聚糖硫酸钠(DSS)诱发的结肠炎。2′-岩藻糖基乳糖 (FL) 和低聚半乳糖 (GOS) 已被证明分别对结肠炎具有预防和改善作用,而有限的研究探讨了 GOS 和 FL 是否对 HFrD 小鼠具有同等的保护或预防作用。在这里,我们评估了 FL 和 GOS 对因喂养 HFrD 而加剧的结肠炎的保护作用,并探讨了其潜在机制。在四只随机 C57BL/6J 雄性小鼠中研究了 DSS 诱导的结肠炎(n= 8 只小鼠/组)。其中,三组接受 HFrD 喂养,两组分别接受 GOS 或 FL 治疗。通过 16S rDNA 基因测序分析肠道微生物组成。使用 qPCR、免疫荧光和蛋白质印迹方法测量肠屏障完整性和炎症通路表达。与 HFrD 组相比,GOS 或 FL 治疗增加了肠道微生物群的 α 多样性,降低了Akkermansia的相对丰度,并分别增加了短链脂肪酸(SCFA)的含量。与HFrD组相比,GOS或FL治疗改善了杯状细胞的丢失和紧密连接蛋白表达的减少,从而改善了肠道屏障的完整性。此外,与 HFrD 组相比,GOS 或 FL 抑制 LPS/TLR4/NF-κB 信号通路和氧化应激,从而抑制炎症级联反应。这些研究结果表明,摄入 GOS 或 FL 可以缓解 HFrD 加剧的结肠炎,但 GOS 和 FL 治疗之间没有观察到显着差异。
更新日期:2023-06-08
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