溃疡性结肠炎
结肠炎
IκB激酶
αBκ
肿瘤坏死因子α
信号转导
谷胱甘肽
葡萄籽提取物
激酶
化学
NFKB1型
NF-κB
氧化应激
药理学
免疫学
医学
生物化学
酶
内科学
病理
转录因子
替代医学
疾病
基因
作者
Yanhong Wang,Bin Ge,Xiaolai Yang,Jing Zhai,Lining Yang,Xiaoxia Wang,Xia Liu,Shi Jin-cheng,Yongjie Wu
标识
DOI:10.1016/j.intimp.2011.05.024
摘要
The aim of this study was to elucidate the molecular mechanisms involved in the therapeutic effects of proanthocyanidins from grape seeds (GSPE) on recurrent ulcerative colitis (UC) in rats. GSPE in doses of 100, 200, and 400mg/kg were intragastrically administered per day for 7 days after recurrent colitis was twice-induced by TNBS. The levels of GSH, as well as the activity of GSH-Px and SOD in colon tissues were measured by biochemical methods. The expression levels of tumor necrosis factor-α (TNF-α) and the nuclear translocation levels of nuclear factor-kappa B (NF-κB) in the colon tissues were measured by enzyme-linked immunosorbent assay methods. Western blotting analysis was used to determine the protein expression levels of inhibitory kappa B-alpha (IκBα), inhibitor kappa B kinase (IKKα/β), phosphorylated IκBα and phosphorylated IKKα/β. GSPE treatment was associated with a remarkable increased the activity of GSH-Px and SOD with GSH levels in TNBS-induced recurrent colitis rats as compared to the model group. GSPE also significantly reduced the expression levels of TNF-α, p-IKKα/β, p-IκBα and the translocation of NF-κB in the colon mucosa. GSPE exerted a protective effect on recurrent colitis in rats by modifying the inflammatory response and promoting damaged tissue repair to improve colonic oxidative stress. Moreover, GSPE inhibited the TNBS-induced inflammatory of recurrent colitis though blocking NF-κB signaling pathways.
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