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白术多糖通过新型长链非编码 RNA ITSN1-OT1 来保护 DSS 诱导的肠道损伤。

Atractylodis macrocephalae polysaccharides protect against DSS-induced intestinal injury through a novel lncRNA ITSN1-OT1.

机构信息

Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Sciences, Zhejiang University, Hangzhou, PR China; Key Laboratory of Animal Nutrition and Feed Science in Eastern China, Ministry of Agriculture, College of Animal Sciences, Zhejiang University, Hangzhou, PR China.

Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou, PR China.

出版信息

Int J Biol Macromol. 2021 Jan 15;167:76-84. doi: 10.1016/j.ijbiomac.2020.11.144. Epub 2020 Nov 25.

DOI:10.1016/j.ijbiomac.2020.11.144
PMID:33248053
Abstract

Many dietary polysaccharides have been shown to protect the intestinal barrier integrity against several noxious stimuli. Previously, we have isolated a polysaccharide RAMPtp from Atractylodis macrocephalae Koidz, and analyzed its structure. However, the effects of RAMPtp on intestinal barrier function have not been investigated. Here, we evaluated the protective effects of RAMPtp on Dextran sulfate sodium (DSS)-induced intestinal epithelial cells (IECs) injury. The findings showed that RAMPtp boosted the proliferation and survival of IECs during DSS stimulation. Furthermore, we found that RAMPtp protected the IECs from injury induced by DSS through maintaining the barrier function and inflammation response. Mechanistically, we identified a novel lncRNA ITSN1-OT1, which was induced by RAMPtp during DSS stimulation. It blocked the nuclear import of phosphorylated STAT2 to prevent the DSS induced decreased expression and structural destroy of tight junction proteins. Hence, the study clarified the protective effects and mechanism of polysaccharides RAMPtp on DSS-induced intestinal barrier dysfunction.

摘要

许多膳食纤维多糖已被证明可以保护肠道屏障的完整性,防止多种有害物质的刺激。先前,我们从白术中分离出一种多糖 RAMPtp,并对其结构进行了分析。然而,RAMPtp 对肠道屏障功能的影响尚未得到研究。在这里,我们评估了 RAMPtp 对葡聚糖硫酸钠(DSS)诱导的肠道上皮细胞(IECs)损伤的保护作用。研究结果表明,RAMPtp 在 DSS 刺激期间促进了 IECs 的增殖和存活。此外,我们发现 RAMPtp 通过维持屏障功能和炎症反应来保护 IECs 免受 DSS 诱导的损伤。在机制上,我们鉴定出一种新型 lncRNA ITSN1-OT1,它是由 RAMPtp 在 DSS 刺激下诱导的。它阻止了磷酸化 STAT2 的核输入,防止了 DSS 诱导的紧密连接蛋白表达和结构破坏。因此,该研究阐明了多糖 RAMPtp 对 DSS 诱导的肠道屏障功能障碍的保护作用及其机制。

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