Abstract：
OBJECTIVE: This study aimed to explore the protective mechanism of chitosan oligosaccharide (COS) against lipopolysaccharide (LPS)-induced inflammatory responses in IEC-6 cells and dextran sodium sulfate (DSS)-induced colitis in mice.
METHODS: The cell inflammation model was constructed by LPS in vitro and enteritis model by DSS in vivo.
RESULTS: Following LPS exposure, IEC-6 cell proliferation significantly decreased, epithelial cell integrity was compromised, and TNF-α and IL-1β levels were increased. However, COS pretreatment reversed these changes. In vivo, DSS-treated mice exhibited evident pathological alterations, including heightened inflammatory levels and significantly decreased expression of tight junction proteins and critical proteins in the Mitogen activated proteins kinase signaling pathway. Nevertheless, COS administration notably reduced inflammatory levels and increased the expression of tight junction proteins and key proteins in the Mitogen activated proteins kinase signaling pathway.
CONCLUSIONS: Our findings suggest that COS safeguards gut barrier integrity by upregulating tight junction proteins through the ERK1/2 signaling pathway. Therefore, COS has emerged as a promising candidate for novel drug interventions against inflammatory bowel disease.
METHODS: The cell inflammation model was constructed by LPS in vitro and enteritis model by DSS in vivo.
RESULTS: Following LPS exposure, IEC-6 cell proliferation significantly decreased, epithelial cell integrity was compromised, and TNF-α and IL-1β levels were increased. However, COS pretreatment reversed these changes. In vivo, DSS-treated mice exhibited evident pathological alterations, including heightened inflammatory levels and significantly decreased expression of tight junction proteins and critical proteins in the Mitogen activated proteins kinase signaling pathway. Nevertheless, COS administration notably reduced inflammatory levels and increased the expression of tight junction proteins and key proteins in the Mitogen activated proteins kinase signaling pathway.
CONCLUSIONS: Our findings suggest that COS safeguards gut barrier integrity by upregulating tight junction proteins through the ERK1/2 signaling pathway. Therefore, COS has emerged as a promising candidate for novel drug interventions against inflammatory bowel disease.
摘要：
目的：本研究旨在探讨壳寡糖(COS)对脂多糖(LPS)诱导的IEC-6细胞炎症反应和葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎的保护机制。
方法：体外用LPS构建细胞炎症模型，体内用DSS构建肠炎模型。
结果：LPS暴露后，IEC-6细胞增殖显著降低,上皮细胞完整性受损，TNF-α和IL-1β水平升高。然而,COS预处理逆转了这些变化。在体内,DSS处理的小鼠表现出明显的病理改变，包括炎症水平升高和丝裂原活化蛋白激酶信号通路中紧密连接蛋白和关键蛋白的表达显著降低。然而，COS给药显著降低炎症水平并增加紧密连接蛋白和丝裂原活化蛋白激酶信号通路中关键蛋白的表达。
结论：我们的研究结果表明，COS通过ERK1/2信号通路上调紧密连接蛋白来保护肠屏障的完整性。因此,COS已成为针对炎症性肠病的新型药物干预的有希望的候选者。
方法：体外用LPS构建细胞炎症模型，体内用DSS构建肠炎模型。
结果：LPS暴露后，IEC-6细胞增殖显著降低,上皮细胞完整性受损，TNF-α和IL-1β水平升高。然而,COS预处理逆转了这些变化。在体内,DSS处理的小鼠表现出明显的病理改变，包括炎症水平升高和丝裂原活化蛋白激酶信号通路中紧密连接蛋白和关键蛋白的表达显著降低。然而，COS给药显著降低炎症水平并增加紧密连接蛋白和丝裂原活化蛋白激酶信号通路中关键蛋白的表达。
结论：我们的研究结果表明，COS通过ERK1/2信号通路上调紧密连接蛋白来保护肠屏障的完整性。因此,COS已成为针对炎症性肠病的新型药物干预的有希望的候选者。
