In this study, we evaluated the effects of tilapia head glycolipids (TH-GLs) on male C57BL/6 mice with inflammatory bowel disease (IBD) induced by dextran sulfate sodium (DSS) and the changes in gut microbiota compared with sulfasalazine. Mice were orally treated with 3% (w/v) DSS or not for 7 days, followed by drug treatment with TH-GLs or sulfasalazine. After treatment, macroscopic colitis symptoms, intestinal epithelial barrier function, inflammatory cytokines, and gut microbiota homeostasis were assessed. Further studies showed that TH-GLs and sulfasalazine showed different influences on the gut microbiota structure. Both sulfasalazine and TH-GLs decreased the DSS-induced enrichment of Gammaproteobacteria and Enterobacteriaceae. However, TH-GLs had a selective increase in the enrichment of Akkermansia, Prevotellaceae, Oscillospira, Allobaculum, Bifidobacterium, and Coprococcus in contrast to sulfasalazine, which selectively increased the enrichment of Dorea, Turicibacter, Bacteroides, Coprobacillus, Mucispirillum, and Dehalobacterium. In addition, both TH-GLs and sulfasalazine relieved body weight loss, and increased the immune organ index, while maintaining the balance between pro-inflammatory and anti-inflammatory cytokines. The results indicate that TH-GLs alleviate DSS-induced IBD in mice by decreasing the abundance of harmful gut microbiota and enhancing the abundance of probiotic gut microbiota. Thus, the mechanism through which TH-GLs inhibit inflammation through gut microbiota is different from that of sulfasalazine. Therefore, TH-GLs stand as potential prebiotics for the treatment of colonic inflammation and related diseases.

中文翻译：

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罗非鱼头糖脂通过调节硫酸葡聚糖钠诱导的结肠炎小鼠的肠道菌群来减轻炎症。

在这项研究中，我们评估了罗非鱼头糖脂（TH-GLs）对硫酸葡聚糖硫酸钠（DSS）诱导的炎症性肠病（IBD）雄性C57BL / 6小鼠的影响以及与柳氮磺吡啶相比肠道菌群的变化。小鼠用3％（w / v）DSS口服治疗或不口服治疗7天，然后用TH-GLs或柳氮磺吡啶治疗。治疗后，评估宏观结肠炎症状，肠上皮屏障功能，炎性细胞因子和肠道菌群稳态。进一步的研究表明，TH-GLs和柳氮磺胺吡啶对肠道菌群结构表现出不同的影响。柳氮磺吡啶和TH-GLs均可降低DSS诱导的丙型变形杆菌和肠杆菌科细菌的富集。但是，TH-GLs选择性地增加了Akkermansia，Prevotellaceae，Oscillospira，Allobaculum，双歧杆菌和副球菌与柳氮磺胺吡啶形成对比，后者可以选择性地增加Dorea，Turicibacter，Bacteroides，Coprobacillus，Muspirspirillum和Dehalobacterium的富集。此外，TH-GLs和柳氮磺胺吡啶均可减轻体重减轻，并增加免疫器官指数，同时保持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。与柳氮磺胺嘧啶相反，柳氮磺胺吡啶可选择性地增加Dorea，Turicibacter，Bacteroides，Coprobacillus，Mucispirillum和Dehalobacterium的富集。此外，TH-GLs和柳氮磺胺吡啶均可减轻体重减轻，并提高免疫器官指数，同时保持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。与柳氮磺胺嘧啶相反，柳氮磺胺吡啶可选择性地增加Dorea，Turicibacter，Bacteroides，Coprobacillus，Mucispirillum和Dehalobacterium的富集。此外，TH-GLs和柳氮磺胺吡啶均可减轻体重减轻，并增加免疫器官指数，同时保持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。杆菌，杆菌，共杆菌，粘螺旋菌和脱盐杆菌。此外，TH-GLs和柳氮磺胺吡啶均可减轻体重减轻，并增加免疫器官指数，同时保持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。杆菌，杆菌，共杆菌，粘螺旋菌和脱盐杆菌。此外，TH-GLs和柳氮磺胺吡啶均可减轻体重减轻，并增加免疫器官指数，同时保持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。并增加免疫器官指数，同时维持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。并增加免疫器官指数，同时维持促炎和抗炎细胞因子之间的平衡。结果表明，TH-GLs通过降低有害肠道菌群的丰度和增强益生菌肠道菌群的丰度来减轻DSS诱导的IBD。因此，TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶的机制不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。TH-GLs通过肠道菌群抑制炎症的机制与柳氮磺胺吡啶不同。因此，TH-GLs是治疗结肠炎症和相关疾病的潜在益生元。