scholarly journals Nuclear Factor Kappa B Regulation of Proinflammatory Cytokines in Human Gestational Tissues In Vitro1

2002 ◽  
Vol 67 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Martha Lappas ◽  
Michael Permezel ◽  
Harry M. Georgiou ◽  
Gregory E. Rice
Keyword(s):  
Proinflammatory Cytokines ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Gestational Tissues

scholarly journals Progesterone Prevents Traumatic Brain Injury-Induced Intestinal Nuclear Factor kappa B Activation and Proinflammatory Cytokines Expression in Male Rats

2007 ◽  
Vol 2007 ◽  
pp. 1-7 ◽  
Author(s):  
Gang Chen ◽  
Jinxin Shi ◽  
Yasuo Ding ◽  
Hongxia Yin ◽  
Chunhua Hang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Proinflammatory Cytokines ◽  
Nuclear Factor Kappa B ◽  
Mucosal Injury ◽  
Therapeutic Benefit ◽  
Binding Activity ◽  
Male Rats ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

We have previously shown that traumatic brain injury (TBI) can induce an upregulation of nuclear factor kappa B (NF-κB) and proinflammatory cytokines in the gut, which play an important role in the pathogenesis of acute gut mucosal injury mediated by inflammation. In this work, we investigated whether progesterone administration modulated intestinal NF-κB activity and proinflammatory cytokines expression after TBI in male rats. As a result, we found that administration of progesterone following TBI could decrease NF-κB binding activity, NF-κB p65 protein expression, and concentrations of interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α) in the gut. TBI-induced damages of gut structure were ameliorated after progesterone injections. The results of the present study suggest that the therapeutic benefit of post-TBI progesterone injections might be due to its inhibitory effects on intestinal NF-κB activation and proinflammatory cytokines expression.

scholarly journals Periploca forrestii saponin ameliorates CIA via suppressing proinflammatory cytokines and nuclear factor kappa-B pathways

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0176672 ◽  
Author(s):  
Chunmei Bao ◽  
Yingqin Liu ◽  
Xin Sun ◽  
Congcong Xing ◽  
Luting Zeng ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Insights antifibrotic mechanism of methyl palmitate: Impact on nuclear factor kappa B and proinflammatory cytokines

2012 ◽  
Vol 258 (1) ◽  
pp. 134-144 ◽  
Author(s):  
Eman M. Mantawy ◽  
Mariane G. Tadros ◽  
Azza S. Awad ◽  
Dina A.A. Hassan ◽  
Ebtehal El-Demerdash
Keyword(s):  
Proinflammatory Cytokines ◽  
Methyl Palmitate ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Overexpression of Helicobacter pylori VacA N-terminal fragment induces proinflammatory cytokine expression and apoptosis in human monocytic cell line through activation of NF-κB

2013 ◽  
Vol 59 (8) ◽  
pp. 523-533 ◽  
Author(s):  
Jing-Jing Luo ◽  
Cun-Yan Li ◽  
Sheng Liu ◽  
Wen Yu ◽  
Shuang-Yang Tang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cell Line ◽  
Proinflammatory Cytokines ◽  
Nuclear Factor Kappa B ◽  
Leukemia Cell Line ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Amino Terminal ◽  
Nuclear Factor Kappa ◽  
Cytokines Secretion

Vacuolating cytotoxin (VacA) is an important virulence factor in the pathogenesis of Helicobacter pylori-related diseases. The aim of this study was to investigate the function of the amino-terminal 476 residue fragment (p52) of VacA and the possible molecular mechanisms responsible for its induction of proinflammatory cytokines secretion and apoptosis. Human acute monocytic leukemia cell line THP-1 was used as an in vitro model to study proinflammatory cytokines secretion and apoptosis induced by transfection of a recombinant plasmid encoding the amino-terminal 476 residue fragment (p52) of VacA. The results showed that VacA p52 overexpression induced the production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), nitric oxide, and reactive oxygen species in THP-1 cells in a time-dependent manner. VacA p52 overexpression also promoted THP-1 cells apoptosis. In addition, VacA p52 triggered the activation of nuclear factor kappa B (NF-κB), indicating a possible mechanism for its induction of proinflammatory cytokines secretion and cell apoptosis. Our study demonstrated that the induction of cytokines secretion and apoptosis by VacA p52 in THP-1 cells could be mediated through activation of nuclear factor kappa B.

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