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.
Highlights
The postoperative infections are a pressing public health challenge, and are primarily attributed to bacteria and viruses
The results showed that bound polyphenols of inner shell (BPIS) and LPS co-treatment significantly inhibited the secretion of pro-inflammatory cytokines, including IL-1β level from 102.51±15.02 pg/ml to 56.44±8.62pg/ml, IL-6 from 48.31±7.15 pg/ ml to 23.06±3.58 pg/ml, IL-8 from 65.36±5.03 pg/ ml to 37.88±4.72 pg/ml and the increased secretion of IL-10 from 13.91±2.84 pg/ml to 23.47±3.41 pg/ml in LPS-induced HT-29 cells, yet no significant change has found in tumor necrosis factor α (TNF-α) (Figure 1A)
We found that BPIS significantly (p
Summary
The postoperative infections are a pressing public health challenge, and are primarily attributed to bacteria and viruses. Lipopolysaccharides, a major component of gram-negative bacterial cell wall play a crucial role to provoke the immune response [1], which lead to chronic inflammation and cancer recurrence colorectal cancer (CRC) [2, 3]. Inflammation is a complex physiological response of body tissues to disease causing irritants, which aims to remove the harmful stimuli and promotes wound healing [4]. Long-term inflammatory reactions are considered as the new malignant phenotype of cancer cells and diffusely approved that chronic inflammation plays a pivotal role in the early stage of cancer [5,6,7]. Controlling LPS-induced inflammatory factors might reduce CRC risk and improve the clinical prospect
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