氧化应激
炎症性肠病
结肠炎
封堵器
炎症
促炎细胞因子
势垒函数
化学
免疫学
药理学
医学
内科学
生物化学
紧密连接
生物
疾病
细胞生物学
作者
Mengqi Li,Renzhi Lv,Chuanzhi Wang,Qi Ge,Hanting Du,Songyi Lin
出处
期刊:Food & Function
[The Royal Society of Chemistry]
日期:2021-01-01
卷期号:12 (23): 11883-11897
被引量:13
摘要
Inflammatory bowel disease (IBD) is a non-specific, chronic inflammatory disease of the intestine. The precise etiology and mechanism underlying the pathogenesis of IBD have not been elucidated. In this study, we investigated the mechanisms through which the Tricholoma matsutake-derived peptide, WFNNAGP, exerts protective effects on the inflammatory response and oxidative stress in a dextran sodium sulfate (DSS)-induced IBD mouse model. WFNNAGP significantly attenuated colitis symptoms in mice, including weight loss, diarrhea, shortened colon, bloody stools, and histopathological changes. WFNNAGP significantly ameliorated the DSS-induced oxidative damage, showing scavenging activity against hydroxyl and DPPH radicals (23.67 ± 4.11% and 34.53 ± 2.45%), increased SOD activity (191.48 ± 4.35 U per mg prot), and decreased MDA activity (1.61 ± 0.24 nmol per mg prot). In addition, WFNNAGP improved the inflammatory response by inhibiting MPO and pro-inflammatory cytokine expression and protected the barrier function by promoting the expression of occludin and ZO-1 in the colon. Western blotting showed that WFNNAGP reduced the inflammatory response by downregulating NF-κB expression and inhibiting the formation and activation of NLRP3 and caspase-1. Thus, WFNNAGP may reduce colonic inflammation in mice by enhancing oxidative defense systems and barrier function and may be a promising candidate for IBD intervention.
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