细胞凋亡
PI3K/AKT/mTOR通路
脂多糖
炎症
活力测定
化学
炎症性肠病
癌症研究
车站3
细胞生物学
分泌物
生物
免疫学
内科学
医学
生物化学
疾病
作者
Lei Li,Guangwen Wan,Bing Han,Zhaowei Zhang
标识
DOI:10.1016/j.biopha.2018.05.072
摘要
Inflammatory bowel disease (IBD) is a chronic and progressive inflammatory condition of colon and small intestine. Echinacoside (ECH) is a phenylethanoid glycoside that possesses various activities, including anti-inflammatory effect. However, the role of ECH in IBD is unknown. The present study aimed to evaluate the effect of ECH on LPS-induced rat intestine epithelial cells and the potential mechanisms. The results showed that LPS inhibited cell viability in time- and dose-dependent manners. ECH treatment attenuated the inhibition effect of LPS on cell viability. ECH alleviated LPS-induced apoptosis of rat intestine epithelial cells. ECH attenuated LPS-induced secretion and mRNA expression of TNF-α and IL-6, but enhanced LPS-induced secretion and mRNA expression of IL-10 and TGF-β1 in IEC-6 cells. The mTOR/STAT3 pathway was activated by LPS, while the activation was inhibited by ECH. Rapamycin, an inhibitor of mTOR, reversed the effect of LPS on rat intestine epithelial cells. In summary, this work suggested that ECH attenuated LPS-induced inflammation and apoptosis in rat intestine epithelial cells via suppressing the mTOR/STAT3 pathway. The findings indicated that ECH might be considered as a potential strategy for the treatment of IBD.
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