Eucommia ulmoides polysaccharide modified nano-selenium effectively alleviated DSS-induced colitis through enhancing intestinal mucosal barrier function and antioxidant capacity.

Eucommia ulmoides polysaccharide modified nano-selenium effectively alleviated DSS-induced colitis through enhancing intestinal mucosal barrier function and antioxidant capacity.
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Eucommia ulmoides多糖改性的纳米 - 丝状糖通过增强肠粘膜屏障功能和抗氧化能力,从而有效地减轻了DSS诱导的结肠炎。

DOI:
10.1186/s12951-023-01965-5
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发表时间:
2023-07-12
影响因子:
10.2
通讯作者:
Dong, Yulan
Dong, Yulan
中科院分区:
工程技术1区
文献类型:
--
作者:
Ye, Ruihua;Guo, Qingyun;Huang, Jiaqiang;Wang, Zixu;Chen, Yaoxing;Dong, Yulan

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溃疡性结肠炎(UC)是目前最常见的炎症性肠病(IBD)。由于其病因多样复杂,目前尚无治愈方法,研究人员也在不断探索新的疗法。近年来,纳米硒颗粒(SeNP)因其优异的生物活性而受到广泛关注。因此,本研究首次采用天然多糖杜仲多糖(EUP)修饰SeNP,得到粒径约为170 nm的EUP-SeNP,并探讨其对3%葡聚糖硫酸钠(DSS)诱导的结肠炎的影响。我们的研究结果表明,结肠炎小鼠的结肠组织学,肠粘膜屏障,炎性细胞因子和肠道微生物组成的改变后,EUP-SeNP治疗。具体而言,还表明EUP-SeNP的口服治疗可以通过恢复体重减轻、降低疾病活动指数(DAI)、增强结肠抗氧化能力和调节肠道微生物组组成来减轻DSS诱导的小鼠结肠炎的程度。此外,我们在肠上皮细胞株中验证了EUP-SeNP的作用机制,表明EUP-SeNP抑制了LPS诱导的肠上皮细胞株TRL-4/NF-κB信号通路的激活。本研究在一定程度上为IBD的治疗提供了参考。
Ulcerative colitis (UC) is currently the most common inflammatory bowel disease (IBD). Due to its diverse and complex causes, there is no cure at present, and researchers are constantly exploring new therapies. In recent years, nano-selenium particle(SeNP) has attracted wide attention due to excellent biological activities. Therefore, in this study, for the first time, we used a natural polysaccharide, Eucommia ulmoides polysaccharide (EUP), modified SeNP to get EUP-SeNP with a size of about 170 nm, and its effect on 3% dextran sulphate sodium (DSS) induced colitis was explored. Our results showed that colon intestinal histology, intestinal mucosal barrier, inflammatory cytokines and intestinal microbiome composition were changed after EUP-SeNP treatment in colitis mice. Specifically, it was also shown that oral treatment of EUP-SeNP could relieve the degree of DSS-induced colitis in mice by restoring weight loss, reducing disease activity index (DAI), enhancing colon antioxidant capacity and regulating intestinal microbiome composition. In addition, we verified the mechanism in intestinal epithelial cell lines, showing that EUP-SeNP inhibited LPS-induced activation of the TRL-4/NF-κB signaling pathway in intestinal epithelial cell lines. To some extend, our study provides therapeutic reference for the treatment of IBD.
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