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以硒化α-D-1,6-葡聚糖形式补充的硒可以改善体内葡聚糖硫酸钠诱导的结肠炎。

Supplementary selenium in the form of selenylation α-D-1,6-glucan ameliorates dextran sulfate sodium induced colitis in vivo.

机构信息

College of Marine Science and Biological Engineering, Qingdao University of Science and Technology, Shandong, Qingdao 266042, China; Shandong Provincial Key Laboratory of biochemical engineering, Shandong, Qingdao 266042, China.

College of Marine Science and Biological Engineering, Qingdao University of Science and Technology, Shandong, Qingdao 266042, China; Shandong Provincial Key Laboratory of biochemical engineering, Shandong, Qingdao 266042, China.

出版信息

Int J Biol Macromol. 2022 Jan 15;195:67-74. doi: 10.1016/j.ijbiomac.2021.11.189. Epub 2021 Dec 8.

DOI:10.1016/j.ijbiomac.2021.11.189
PMID:34896151
Abstract

The deficiency of selenium has been found in clinical IBD patients and supplementation selenium is recognized as beneficial for colitis treatment. In this study, an organic selenium compound-selenylation α-D-1,6-glucan (sCPA) was prepared, and the effect of sCPA on DSS induced colitis mice was investigated. The results suggested that sCPA prevented the weight loss, colon length shortening, and stool loose of colitis mice. It protected colon mucosal barrier by promoting tight junction protein ZO-1 and Occludin expression. Moreover, sCPA reduced oxidative stress via regulating SOD and MDA levels, and decreased the contents of inflammatory proteins NF-κB and NLRP3 and adjusted TNF-α, IFN-γ, IL-1β, and IL-10 inflammatory cytokines. Furthermore, sCPA repaired intestinal microbiota composition especially Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria that altered by DSS in colitis mice. Meanwhile, SCFAs produced by gut microbiota were restored by sCPA close to the level in the normal group. In conclusion, these findings indicated that the sCPA might be a potential dietary selenium supplementation for the prevention and treatment of colitis.

摘要

研究发现,临床 IBD 患者存在硒缺乏,补充硒被认为有益于结肠炎的治疗。本研究制备了一种有机硒化合物-硒化α-D-1,6-葡聚糖(sCPA),并研究了 sCPA 对 DSS 诱导的结肠炎小鼠的作用。结果表明,sCPA 可预防结肠炎小鼠的体重减轻、结肠缩短和粪便松散。它通过促进紧密连接蛋白 ZO-1 和 Occludin 的表达来保护结肠黏膜屏障。此外,sCPA 通过调节 SOD 和 MDA 水平来减轻氧化应激,并降低炎症蛋白 NF-κB 和 NLRP3 的含量,调节 TNF-α、IFN-γ、IL-1β 和 IL-10 等炎症细胞因子。此外,sCPA 修复了肠道微生物群落的组成,特别是 DSS 改变的拟杆菌门、厚壁菌门、变形菌门和放线菌门。同时,sCPA 使由肠道微生物群产生的 SCFAs 恢复到接近正常组的水平。总之,这些发现表明,sCPA 可能是预防和治疗结肠炎的一种潜在的膳食硒补充剂。

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