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Almond polysaccharides inhibit DSS-induced inflammatory response in ulcerative colitis mice through NF-κB pathway

溃疡性结肠炎 NF-κB 多糖 炎症反应 结肠炎 炎症 化学 炎症性肠病 NFKB1型 免疫学 医学 生物化学 基因 病理 疾病 转录因子
作者
Yanqi Peng,Jiayi Zhu,Yingshuo Li,Xiqing Yue,Yanyu Peng
出处
期刊:International Journal of Biological Macromolecules [Elsevier BV]
卷期号:: 136206-136206 被引量:10
标识
DOI:10.1016/j.ijbiomac.2024.136206
摘要

Ulcerative colitis (UC), a type of inflammatory bowel disease (IBD), is a chronic recurrent inflammatory disease of the colon. Our previous findings demonstrated that almond polysaccharide (AP-1) exhibits significant anti-inflammatory activity in vitro. Therefore, this study aimed to explore the ameliorative effect of AP-1 on dextrose sodium sulfate (DSS)-induced UC mice and to elucidate its possible mechanism of action. By observing changes in body weight, fecal viscosity, stool blood, disease activity index, and colon length, we found that AP-1 attenuated inflammation. It inhibited TNF-α, IL-1β, and IL-6 while boosting anti-inflammatory IL-10 levels. Histomorphologically, AP-1 protected against DSS-induced colonic tissue damage by reducing inflammatory cell infiltration and mucosal injury. It also lowered myeloperoxidase (MPO) and NO while increasing total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) in colonic tissues. Moreover, using the Western blot technique, AP-1 was shown to inhibit the phosphorylation of p65 and IκB-α proteins in the NF-κB/iNOS/COX2 signaling pathway and down-regulate the expression of inflammation-associated proteins COX2 and iNOS, thus slowing down and ameliorating inflammatory processes. Therefore, the safe and effective beneficial effects of AP-1 make it a promising therapeutic strategy for relieving IBD, especially UC.
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