Anti-inflammatory effects of millet bran derived-bound polyphenols in LPS-induced HT-29 cell via ROS/miR-149/Akt/NF-κB signaling pathway
Metrics: PDF 1637 views | HTML 3424 views | ?
Jiangying Shi1,*, Shuhua Shan1,*, Hanqing Li1,2, Guisheng Song3 and Zhuoyu Li1,2
1Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, China
2College of Life Science, Shanxi University, Taiyuan 030006, China
3Department of Medicine, Division of Gastroenterology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
*These authors have contributed equally to this work
Zhuoyu Li, email: [email protected]
Keywords: foxtail millet bran, bound polyphenols, ROS, miR-149, anti-inflammation
Received: December 22, 2016 Accepted: June 05, 2017 Published: August 12, 2017
The pro-inflammatory and anti-inflammatory maladjustment has been acknowledged as one of the chief causations of inflammatory diseases and even cancers. Previous studies showed that plant-derived polyphenolic compounds were the most potent anti-oxidant and anti-inflammatory agents among all natural compounds. The present study indicates that bound polyphenols of inner shell (BPIS) from foxtail millet bran can display anti-inflammatory effects in LPS-induced HT-29 cells and in nude mice. Mechanistically, BPIS restrained the level of various pro-inflammatory cytokines (IL-1β, IL-6, IL-8), and enhanced the expression level of anti-inflammatory cytokine (IL-10) by blocking the nuclear factor-kappaB (NF-κB)-p65 nuclear translocation. Further, we found the elevated miR-149 expression by BPIS-induced ROS accumulation, directly targeted the Akt expression to block NF-κB nuclear translocation. Taken together, these novel findings provide new insights into the development of BPIS as an anti-inflammatory agent via the signaling cascade of ROS/miR-149/Akt/NF-κB axis.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.