脂多糖
炎症
封堵器
势垒函数
紧密连接
化学
炎症性肠病
碳酸钙-2
山奈酚
分泌物
免疫学
槲皮素
细胞生物学
生物
内科学
医学
生物化学
体外
抗氧化剂
疾病
作者
Yifei Bian,Yuanyang Dong,Jingjing Sun,Meng Sun,Qihang Hou,Yujiao Lai,Bingkun Zhang
标识
DOI:10.1021/acs.jafc.9b06294
摘要
Inflammatory bowel disease (IBD) is a chronic inflammatory disease of intestinal mucosa and submucosa, characterized by the disruption of the intestinal epithelial barrier, increased production of inflammatory mediators, and excessive tissue injury. Intestinal epithelial cells, as well as microvascular endothelial cells, play important roles in IBD. To study the potential effects of kaempferol in IBD progress, we established a novel epithelial–endothelial cells coculture model to investigate the intestinal inflammation and barrier function. Data demonstrated an obvious increased transepithelial electrical resistance (TEER) (1222 ± 60.40 Ω cm2 vs 1371 ± 38.77 Ω cm2), decreased flux of FITC (180.8 ± 20.06 μg/mL vs 136.7 ± 14.78 μg/mL), and up-regulated occludin and claudin-2 expression in Caco-2 that was specifically cocultured with endothelial cells. Meanwhile, 80 μM kaempferol alleviated the drop of TEER, the increase of FITC flux, and the overexpression of interleukin-8 (IL-8) induced by 1 μg/mL lipopolysaccharide (LPS). Additionally, kaempferol also ameliorated the LPS-induced decrease of protein expression of zonula occludens-1 (ZO-1), occludin, and claudin-2, together with the inhibited protein expressions of the phosphorylation level of NF-κB and I-κB induced by LPS. Our results suggest that kaempferol alleviates the IL-8 secretion and barrier dysfunction of the Caco-2 monolayer in the LPS-induced epithelial–endothelial coculture model via inhibiting the NF-κB signaling pathway activation.
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