Xu Yingyin, Feng Huiyu, Zhang Zhiyuan, Zhang Qian, Tang Jie, Zhou Jie, Wang Yong, Peng Weihong
Sichuan Institute of Edible Fungi, Chengdu 610066, China.
National-Local Joint Engineering Laboratory of Breeding and Cultivation of Edible and Medicinal Fungi, Chengdu 610066, China.
Foods. 2023 Feb 3;12(3):669. doi: 10.3390/foods12030669.
, a type of edible fungus, is beneficial for intestinal health. However, the mechanisms by which polysaccharides derived from . contribute to the integrity of the intestinal barrier have been little investigated. In the present study, 40 C57BL/6J mice were assigned into five groups: (1) Normal; (2) Dextran sulfate sodium (DSS)Administration; (3) DSS + Uncapped polysaccharides; (4) DSS + Low microcapsules; (5) DSS + High microcapsules. After one week of administration of polysaccharides, all mice, excluding the Normal group, had free access to the drinking water of 3.5% DSS for seven days. Serum and feces were then taken for analysis. Scanning electron microscopy analysis indicated the structure of the micro-capped polysaccharides with curcumin was completed with a rough surface, which differs from the uncapped polysaccharides. Noticeably, polysaccharides enhanced intestinal barrier integrity as evidenced by increasing the protein levels of Claudin-1, ZO-1 and ZO-2. Low-capped polysaccharides mitigated the DSS-induced oxidative stress by increasing catalase (CAT) concentration and decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) concentrations. Besides, DSS treatment caused a disturbance of inflammation and the contents of IL-1β, IL-6, TNF-α and CRP were downregulated and the contents of IL-4, IL-10 and IFN-γ were upregulated by polysaccharides. Research on the potential mechanisms indicated that polysaccharides inhibited the DSS-triggered activation of NF-κB signaling. Moreover, the JAK/STAT1 and MAPK pathways were suppressed by polysaccharides in DSS-challenged mice, with Lcap showing the strongest efficacy. 16S rDNA amplicon sequencing revealed that the richness and diversity of the microbial community were reshaped by polysaccharide ingestion. Therefore, our study substantiated that polysaccharides exhibited protective effects against colitis mice by reshaping the intestinal microbiome and maintaining the balance of intestinal barrier integrity, antioxidant capacity and colonic inflammation through regulation of the NF-κB-STAT1-MAPK axis.
[某种食用菌名称]是一种食用菌，对肠道健康有益。然而，源自[该食用菌名称]的多糖有助于肠道屏障完整性的机制鲜有研究。在本研究中，40只C57BL/6J小鼠被分为五组：(1)正常组；(2)葡聚糖硫酸钠（DSS）给药组；(3) DSS + 未包封多糖组；(4) DSS + 低包封微胶囊组；(5) DSS + 高包封微胶囊组。给予[该食用菌名称]多糖一周后，除正常组外，所有小鼠自由饮用3.5% DSS的饮用水7天。然后采集血清和粪便进行分析。扫描电子显微镜分析表明，含姜黄素的微包封多糖结构完整，表面粗糙，这与未包封多糖不同。值得注意的是，[该食用菌名称]多糖通过增加Claudin-1、ZO-1和ZO-2的蛋白水平，增强了肠道屏障的完整性。低包封多糖通过增加过氧化氢酶（CAT）浓度、降低丙二醛（MDA）和髓过氧化物酶（MPO）浓度，减轻了DSS诱导的氧化应激。此外，DSS处理导致炎症紊乱，[该食用菌名称]多糖下调了IL-1β、IL-6、TNF-α和CRP的含量，上调了IL-4、IL-10和IFN-γ的含量。对潜在机制的研究表明，[该食用菌名称]多糖抑制了DSS触发的NF-κB信号通路的激活。此外，在DSS攻击的小鼠中，[该食用菌名称]多糖抑制了JAK/STAT1和MAPK通路，低包封微胶囊（Lcap）显示出最强的效果。16S rDNA扩增子测序显示，摄入[该食用菌名称]多糖重塑了微生物群落的丰富度和多样性。因此，我们的研究证实，[该食用菌名称]多糖通过重塑肠道微生物群，并通过调节NF-κB-STAT1-MAPK轴维持肠道屏障完整性、抗氧化能力和结肠炎症的平衡，对结肠炎小鼠具有保护作用。
