封堵器
超氧化物歧化酶
氧化应激
谷胱甘肽
化学
丙二醛
势垒函数
丙烯酰胺
TLR4型
药理学
免疫印迹
肠粘膜
过氧化氢酶
肠道通透性
炎症
生物化学
紧密连接
免疫学
生物
内科学
医学
信号转导
酶
细胞生物学
有机化学
聚合物
基因
共聚物
作者
Dan Su,Aitong Lei,Chunchao Nie,Yi Chen
标识
DOI:10.1016/j.fct.2022.113548
摘要
The potential mechanism for the protective effect of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrylamide (AA) induced intestinal damage in mice was explored. Results showed that PSG-1 pretreatment prevented AA-induced injury by decreasing intestinal permeability and serum D-lactate acid (D-Lac) levels and increasing the number of small intestinal goblet cells and IgA secreting cells. In addition, PSG-1 pretreatment effectively reduced malondialdehyde (MDA) level and raised superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) activities in the intestine. Furthermore, PSG-1 administration decreased the levels of pro-inflammatory factors including IL-1β, TNF-α, and IL-6, while the anti-inflammatory factor IL-10 was elevated. Meanwhile, PSG-1 could increase the performance of tight junction (TJ) proteins such as Occludin, Claudin-1 and ZO-1. Moreover, according to the isobaric tag for relative and absolute quantitation (iTRAQ) and Western blot results, PSG-1 could reduce AA-induced intestinal injury through TLR4/MyD88/NF-κB signaling pathway. Overall, the present study suggested that PSG-1 protected intestinal permeability and barrier function in mice via reducing inflammation and oxidative stress, and effectively prevented AA-induced intestinal injury in mice.
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