Echinacoside alleviated LPS-induced cell apoptosis and inflammation in rat intestine epithelial cells by inhibiting the mTOR/STAT3 pathway

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
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier BV]
卷期号:104: 622-628 被引量:134
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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