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

Abstract

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.

• Authors: Lei Li, Guangwen Wan, Bing Han, Zhaowei Zhang
• Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (Biomed Pharmacother) Vol. 104 Pg. 622-628 (Aug 2018) ISSN: 1950-6007 [Electronic] France
• PMID: 29803175 (Publication Type: Journal Article)
• Copyright: Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Chemical References

• Glycosides
• Lipopolysaccharides
• STAT3 Transcription Factor
• Stat3 protein, rat
• Transforming Growth Factor beta1
• Interleukin-10
• mTOR protein, rat
• TOR Serine-Threonine Kinases
• echinacoside
• Sirolimus

Topics

• Animals
• Apoptosis (drug effects)
• Cell Survival (drug effects)
• Epithelial Cells (drug effects, metabolism)
• Glycosides (pharmacology)
• Inflammation (chemically induced, drug therapy, metabolism)
• Interleukin-10 (metabolism)
• Intestinal Mucosa (metabolism)
• Intestines (drug effects)
• Lipopolysaccharides (pharmacology)
• Rats
• STAT3 Transcription Factor (metabolism)
• Signal Transduction (drug effects)
• Sirolimus (pharmacology)
• TOR Serine-Threonine Kinases (metabolism)
• Transforming Growth Factor beta1 (metabolism)