Ameliorating effects of Geranium Koreanum kom on esophageal damage in reflux esophagitis via nuclear factor-κB signaling-mediated anti-inflammatory activities

2019 ◽  
Vol 15 (61) ◽  
pp. 290
Author(s):  
ByungKil Choo ◽  
HyeonHwa Nam ◽  
Li Nan
Keyword(s):  
Reflux Esophagitis ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Anti Inflammatory

scholarly journals Nuclear Factor-κB Inhibitors as Potential Novel Anti-Inflammatory Agents for the Treatment of Immune Glomerulonephritis

2002 ◽  
Vol 161 (4) ◽  
pp. 1497-1505 ◽  
Author(s):  
Oscar López-Franco ◽  
Yusuke Suzuki ◽  
Guillermo Sanjuán ◽  
Julia Blanco ◽  
Purificación Hernández-Vargas ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Anti Inflammatory

scholarly journals Biological Evaluation of Alkyl Triphenylphosphonium Ostruthin Derivatives as Potential Anti-Inflammatory Agents Targeting the Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

BioChem ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 107-121
Author(s):  
Nghia Trong Vo ◽  
Eiichi Kusagawa ◽  
Kaori Nakano ◽  
Chihiro Moriwaki ◽  
Yasunobu Miyake ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Human Lung ◽  
A549 Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Human Lung Adenocarcinoma ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Lung Adenocarcinoma A549

Ostruthin (6-geranyl-7-hydroxycoumarin) is one of the constituents isolated from Paramignya trimera and has been classified as a simple coumarin. We recently reported the synthesis of alkyl triphenylphosphonium (TPP) derivatives from ostruthin and evaluated their anticancer activities. In the present study, we demonstrated that alkyl TPP ostruthin derivatives inhibited the up-regulation of cell-surface intercellular adhesion molecule-1 (ICAM-1) in human lung adenocarcinoma A549 cells stimulated with tumor necrosis factor-α (TNF-α) without affecting cell viability, while ostruthin itself exerted cytotoxicity against A549 cells. The heptyl TPP ostruthin derivative (termed OS8) attenuated the up-regulation of ICAM-1 mRNA expression at concentrations higher than 40 µM in TNF-α-stimulated A549 cells. OS8 inhibited TNF-α-induced nuclear factor κB (NF-κB)-responsive luciferase reporter activity at concentrations higher than 40 µM, but did not affect the translocation of the NF-κB subunit RelA in response to the TNF-α stimulation at concentrations up to 100 µM. A chromatin immunoprecipitation assay showed that OS8 at 100 µM prevented the binding of RelA to the ICAM-1 promoter. We also showed that OS8 at 100 µM inhibited the TNF-α-induced phosphorylation of RelA at Ser 536. Moreover, the TNF-α-induced phosphorylation of an inhibitor of NF-κB α and extracellular signal-regulated kinase was reduced by OS8. These results indicate that OS8 has potential as an anti-inflammatory agent that targets the NF-κB signaling pathway.

scholarly journals Mapping the Interaction of B Cell Leukemia 3 (BCL-3) and Nuclear Factor κB (NF-κB) p50 Identifies a BCL-3-mimetic Anti-inflammatory Peptide

2015 ◽  
Vol 290 (25) ◽  
pp. 15687-15696 ◽  
Author(s):  
Patricia E. Collins ◽  
Gianluca Grassia ◽  
Amy Colleran ◽  
Patrick A. Kiely ◽  
Armando Ialenti ◽  
...  
Keyword(s):  
B Cell ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Cell Leukemia ◽  
B Cell Leukemia ◽  
Anti Inflammatory

Incensole Acetate, a Novel Anti-Inflammatory Compound Isolated fromBoswelliaResin, Inhibits Nuclear Factor-κB Activation

2007 ◽  
Vol 72 (6) ◽  
pp. 1657-1664 ◽  
Author(s):  
Arieh Moussaieff ◽  
Esther Shohami ◽  
Yoel Kashman ◽  
Ester Fride ◽  
M. Lienhard Schmitz ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Anti Inflammatory

β-Adrenergic agonists exert their “anti-inflammatory” effects in monocytic cells through the IκB/NF-κB pathway

2000 ◽  
Vol 279 (4) ◽  
pp. L675-L682 ◽  
Author(s):  
Pierre Farmer ◽  
Jérôme Pugin
Keyword(s):  
Mononuclear Cells ◽  
Nuclear Translocation ◽  
Nuclear Factor Κb ◽  
Late Time ◽  
Nuclear Factor ◽  
Adrenergic Agonists ◽  
Time Points ◽  
Human Mononuclear Cells ◽  
Anti Inflammatory ◽  
Factor Α

In addition to their well-studied bronchodilatory and cardiotonic effects, β-adrenergic agonists carry anti-inflammatory properties by inhibiting cytokine production by human mononuclear cells. In a model of human promonocytic THP-1 cells stimulated with lipopolysaccharide (LPS), we showed that β-agonists inhibited tumor necrosis factor-α and interleukin-8 production predominantly via the β2-adrenergic receptor through the generation of cAMP and activation of protein kinase A. This effect was reproduced by other cAMP-elevating agents such as prostaglandins and cAMP analogs. Activation and nuclear translocation of the transcription factor nuclear factor-κB induced by LPS were inhibited with treatment with β-agonists, an effect that was prominent at late time points (>1 h). Although the initial IκB-α degradation induced by LPS was minimally affected by β-agonists, the latter induced a marked rebound of the cytosolic IκB-α levels at later time points (>1 h), accompanied by an increased IκB-α cytoplasmic half-life. This potentially accounts for the observed nuclear factor-κB sequestration in the cytoplasmic compartment. We postulate that the anti-inflammatory effects of β-agonists reside in their capacity to increase cytoplasmic concentrations of IκB-α, possibly by decreasing its degradation.

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