Oncotarget

Research Papers:

Anti-inflammatory effects of millet bran derived-bound polyphenols in LPS-induced HT-29 cell via ROS/miR-149/Akt/NF-κB signaling pathway

Jiangying Shi, Shuhua Shan, Hanqing Li, Guisheng Song and Zhuoyu Li _

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Oncotarget. 2017; 8:74582-74594. https://doi.org/10.18632/oncotarget.20216

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Abstract

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

Correspondence to:

Zhuoyu Li, email: lzy@sxu.edu.cn

Keywords: foxtail millet bran, bound polyphenols, ROS, miR-149, anti-inflammation

Received: December 22, 2016    Accepted: June 05, 2017    Published: August 12, 2017

ABSTRACT

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.


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