Jia Jinhui, Zhang Panpan, Zhang Chenxi, Jiang Guoping, Zheng Weiyun, Song Shuang, Ai Chunqing
School of Food Science and Technology; National Engineering Research Center of Seafood, Dalian Polytechnic University, Dalian 116034, P. R. China.
National & Local Joint Engineering Laboratory for Marine Bioactive Polysaccharide Development and Application, Dalian Polytechnic University, Dalian 116034, P. R. China.
Food Funct. 2021 Nov 15;12(22):11351-11365. doi: 10.1039/d1fo02431k.
Due to potential side effects of current drugs in colitis treatment, polysaccharides with anti-inflammatory activities can be considered as alternative molecules for colitis treatment. Sulfated polysaccharide from pacific abalone (AGSP) reduced the level of lipopolysaccharides (LPS) and increased the production of short chain fatty acids in the colon of mice, and it reduced the levels of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α and increased the IL-10 level in cell models, suggesting that it can be used as a probiotic agent to inhibit intestinal inflammation. Furthermore, AGSP reduced the disease activity index and intestinal damage, improved the mucosal immune response, and inhibited oxidative damage in mice with DSS-induced acute and chronic colitis, which can be associated with modulation of the NF-κB signaling pathway and gut microbiota. AGSP regulated the structure of the gut microbiota and reduced the level of that had positive correlation with the colitis symptoms. The result showed that AGSP may inhibit mucin degradation by the change of the polysaccharide utilization strategy, which can protect intestinal barrier integrity. This study is useful to understand the mechanism by which AGSP ameliorates colitis and related diseases and promotes further development of AGSP.
由于目前用于结肠炎治疗的药物存在潜在副作用,具有抗炎活性的多糖可被视为结肠炎治疗的替代分子。太平洋鲍鱼硫酸化多糖(AGSP)降低了小鼠结肠中脂多糖(LPS)的水平,增加了短链脂肪酸的产生,并且在细胞模型中降低了白细胞介素(IL)-6、IL-1β和肿瘤坏死因子(TNF)-α的水平,提高了IL-10水平,表明它可作为一种益生菌剂来抑制肠道炎症。此外,AGSP降低了疾病活动指数和肠道损伤,改善了黏膜免疫反应,并抑制了葡聚糖硫酸钠(DSS)诱导的急性和慢性结肠炎小鼠的氧化损伤,这可能与核因子κB(NF-κB)信号通路和肠道微生物群的调节有关。AGSP调节了肠道微生物群的结构,并降低了与结肠炎症状呈正相关的[此处原文缺失相关内容]水平。结果表明,AGSP可能通过改变多糖利用策略来抑制粘蛋白降解,从而保护肠道屏障完整性。本研究有助于理解AGSP改善结肠炎及相关疾病的机制,并促进AGSP的进一步开发。