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银耳多糖通过抑制炎症和增强肠道上皮屏障功能来改善溃疡性结肠炎。

Tremella fuciformis polysaccharides ameliorated ulcerative colitis via inhibiting inflammation and enhancing intestinal epithelial barrier function.

机构信息

School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong, PR China.

Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an 223002, Jiangsu, PR China.

出版信息

Int J Biol Macromol. 2021 Jun 1;180:633-642. doi: 10.1016/j.ijbiomac.2021.03.083. Epub 2021 Mar 17.

Abstract

The purpose of this paper was to explore the therapeutic effect and underlying mechanism of Tremella fuciformis polysaccharides (TFP) on ulcerative colitis (UC) based on dextran sodium sulfate (DSS)-induced mice UC model and lipopolysaccharide (LPS)-stimulated Caco-2 cells model. The results firstly indicated that TFP can significantly alleviate the symptoms and signs of the DSS-induced mice UC model, which manifests as improvement of body weight loss, increase of colon length, decrease of colon thickness and reduction of intestinal permeability. Then, results from histopathological and electron microscope analysis further implied that TFP could dramatically reduce inflammatory cells infiltration and restore intestinal epithelial barrier integrity. In addition, the experiments of LPS-stimulated Caco-2 cells model in vitro also further confirmed that TFP could markedly inhibit the expressions of pro-inflammatory cytokines and increase related genes or proteins expressions of intestinal barrier and mucus barrier. Taken together, these data suggested that TFP has a significant therapeutic effect on DSS-induced UC model, and its mechanisms are closely linked to the inhibition of inflammation and the restoration of intestinal barrier and mucus barrier function. These beneficial effects may make TFP a promising drug to be used in alleviating UC.

摘要

本文旨在基于葡聚糖硫酸钠(DSS)诱导的小鼠溃疡性结肠炎(UC)模型和脂多糖(LPS)刺激的 Caco-2 细胞模型,探讨银耳多糖(TFP)对溃疡性结肠炎的治疗作用及其潜在机制。结果首先表明,TFP 能显著缓解 DSS 诱导的小鼠 UC 模型的症状和体征,表现为体重减轻、结肠长度增加、结肠厚度降低和肠通透性降低的改善。然后,组织病理学和电子显微镜分析的结果进一步表明,TFP 能显著减少炎症细胞浸润,恢复肠上皮屏障完整性。此外,体外 LPS 刺激的 Caco-2 细胞模型实验也进一步证实,TFP 能显著抑制促炎细胞因子的表达,并增加肠屏障和黏液屏障相关基因或蛋白的表达。综上所述,这些数据表明,TFP 对 DSS 诱导的 UC 模型具有显著的治疗作用,其机制与抑制炎症和恢复肠屏障及黏液屏障功能密切相关。这些有益作用可能使 TFP 成为一种有前途的药物,用于缓解 UC。

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