特里夫
髓过氧化物酶
化学
超氧化物歧化酶
丙二醛
谷胱甘肽过氧化物酶
下调和上调
结肠炎
溃疡性结肠炎
TLR4型
炎症
谷胱甘肽
NF-κB
氧化应激
信号转导
药理学
内科学
免疫学
生物化学
医学
先天免疫系统
受体
Toll样受体
酶
基因
疾病
作者
Yaping Li,Pan Xiao,Mingyuan Yin,Cuiping Li,Lirong Han
标识
DOI:10.1021/acs.jafc.1c05128
摘要
The preventive effect and molecular mechanism of lycopene (LP) in dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were evaluated. Compared to the DSS group, the LP prevention groups not only significantly inhibited the DSS-induced weight loss, decreased the disease activity index (DAI) score, increased the colon length, and improved inflammation in the colon but also significantly increased the levels of superoxide dismutase (SOD),catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) in the colon and reduced inflammatory cytokine, myeloperoxidase (MPO), and malondialdehyde (MDA) levels. Notably, when compared to the DSS group, the protein expression levels of TLR4, TRIF, and p-NF-κB p65 in the mice colon tissue were downregulated and those of tight junction-related proteins were upregulated in the LP + DSS group, with the most significant effect observed in the 10 mg/kg LP + DSS group. These results confirmed that the upregulation of tight junction-related protein expression after blocking the TLR4/TRIF/NF-κB signaling pathway may be one of the mechanisms through which LP prevents UC.
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