Selenium nanoparticles decorated with Ulva lactuca polysaccharide potentially attenuate colitis by inhibiting NF-κB mediated hyper inflammation.

Selenium nanoparticles decorated with Ulva lactuca polysaccharide potentially attenuate colitis by inhibiting NF-κB mediated hyper inflammation.
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用石莼多糖装饰的硒纳米颗粒可通过抑制 NF-κB 介导的过度炎症来减轻结肠炎

DOI:
10.1186/s12951-017-0252-y
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发表时间:
2017-03-07
影响因子:
10.2
通讯作者:
Huang Z
Huang Z
中科院分区:
工程技术1区
文献类型:
--
作者:
Zhu C;Zhang S;Song C;Zhang Y;Ling Q;Hoffmann PR;Li J;Chen T;Zheng W;Huang Z

文献摘要

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硒是一种必需的微量营养素,也是公认的营养抗氧化剂。低硒水平会加剧炎症性肠病的进展,这涉及到消化道的高度炎症。硒纳米颗粒(SeNPs)具有抗炎活性,且毒性低,特别是在天然生物化合物的修饰下。在此,我们探讨了石笋多糖(ULP)修饰的SeNPs对小鼠急性结肠炎模型的有益作用。我们构建了平均直径约130 nm的包被ULP的SeNPs(ULP-SeNPs),并对其稳定性和均一性进行了研究。补充ULP-SeNPs(0.8ppm Se)对DSS诱导的小鼠急性结肠炎有显著的保护作用,包括减轻体重减轻和结肠炎性损伤。ULP-SeNPs可改善巨噬细胞的浸润,其证据是结肠组织切片中CD68水平降低。ULP-SeNPs的抗炎作用涉及对IL-6和肿瘤坏死因子-α等细胞因子的调节。机制上,ULP-SeNPs通过抑制核因子-κB的核转位来抑制巨噬细胞的激活,核转位驱动这些促炎细胞因子的转录。ULP-SeNPs补充剂可能通过其抗炎作用为减轻急性结肠炎的症状提供治疗潜力。本文的在线版本(doi:10.1186/s12951-0170252-y)包含补充材料,授权用户可以使用。
Selenium (Se) is an essential micronutrient trace element and an established nutritional antioxidant. Low Se status exacerbates inflammatory bowel diseases progression, which involves hyper inflammation in the digestive tract. Se nanoparticles (SeNPs) exhibit anti-inflammatory activity accompanied by low toxicity, especially when decorated with natural biological compounds. Herein, we explored the beneficial effects of SeNPs decorated with Ulva lactuca polysaccharide (ULP) in mice subjected to the acute colitis model. We constructed SeNPs coated with ULP (ULP-SeNPs) in average diameter ~130 nm and demonstrated their stability and homogeneity. Supplementation with ULP-SeNPs (0.8 ppm Se) resulted in a significant protective effect on DSS-induced acute colitis in mice including mitigation of body weight loss, and colonic inflammatory damage. ULP-SeNPs ameliorated macrophage infiltration as evidenced by decreased CD68 levels in colon tissue sections. The anti-inflammatory effects of ULP-SeNPs were found to involve modulation of cytokines including IL-6 and TNF-α. Mechanistically, ULP-SeNPs inhibited the activation of macrophages by suppressing the nuclear translocation of NF-κB, which drives the transcription of these pro-inflammatory cytokines. ULP-SeNPs supplementation may offer therapeutic potential for reducing the symptoms of acute colitis through its anti-inflammatory actions. The online version of this article (doi:10.1186/s12951-017-0252-y) contains supplementary material, which is available to authorized users.