Justicidin A Inhibits the Transport of Tumor Necrosis Factor-α to Cell Surface in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages

2004 ◽  
Vol 65 (5) ◽  
pp. 1063-1069 ◽  
Author(s):  
Lo-Ti Tsao ◽  
Chun-Nan Lin ◽  
Jih-Pyang Wang
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Surface ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Alpha-Lipoic Acid Suppresses Extracellular Histone-Induced Release of the Infammatory Mediator Tumor Necrosis Factor-α by Macrophages

2017 ◽  
Vol 42 (6) ◽  
pp. 2559-2568 ◽  
Author(s):  
Ping Chang ◽  
Juan Liu ◽  
Ying Yu ◽  
Shao-Ye Cui ◽  
Zhen-Hui Guo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathways ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Raw 264.7 ◽  
Alpha Lipoic Acid ◽  
Tnf Α ◽  
Extracellular Histones ◽  
Factor Α ◽  
Necrosis Factor

Background/Aims: This study investigated signaling pathways via which extracellular histones induce the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) release from the macrophage cell line RAW 264.7 and the anti-inflammatory efficacy of the antioxidant alpha-lipoic acid (ALA). Methods: ELISA and western blotting analyses were conducted to detect the release of TNF-α from histone-stimulated RAW 264.7 macrophages and the associated phospho-activation of MAPKs (ERK and p38) and NF-κB p65. The effects of ALA on the release of TNF-α and phospho-activation of the MAPKs and NF-κB p65 were studied. P < 0.05 was considered statistically significant. Results: Extracellular histones dose-dependently induced TNF-α release from RAW 264.7 cells and increased the phosphorylation of p38, ERK, and NF-κB p65. TNF-α release was markedly suppressed by p38, ERK, and NF-kB inhibitors. ALA reduced histone-induced TNF-α release, ERK/p38 MAPK activation, and NF-kB activation without affecting macrophage viability. Conclusion: Histones induce TNF-α release from macrophages by activating the MAPK and NF-kB signaling pathways, while ALA suppresses this response by inhibiting ERK, p38 and NF-kB. These findings identify potentially critical inflammatory signaling pathways in sepsis and molecular targets for sepsis treatment.

scholarly journals Size-Dependent Effect of Silver Nanoparticles on the Tumor Necrosis Factor α-Induced DNA Damage Response

2019 ◽  
Vol 20 (5) ◽  
pp. 1038 ◽  
Author(s):  
Alaa Fehaid ◽  
Akiyoshi Taniguchi
Keyword(s):  
Dna Damage ◽  
Silver Nanoparticles ◽  
Tumor Necrosis Factor ◽  
Cell Surface ◽  
Dna Damage Response ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Damage Response ◽  
Factor Α ◽  
Necrosis Factor

Silver nanoparticles (AgNPs) are widely used in many consumer products due to their anti-inflammatory properties. Therefore, the effect of exposure to AgNPs should be investigated in diseased states in addition to healthy ones. Tumor necrosis factor-α (TNFα) is a major cytokine that is highly expressed in many diseased conditions, such as inflammatory diseases, sepsis, and cancer. We investigated the effects of two different sizes of AgNPs on the TNFα-induced DNA damage response. Cells were exposed to 10 and 200 nm AgNPs separately and the results showed that the 200 nm AgNPs had a lower cytotoxic effect with a higher percent of cellular uptake compared to the 10 nm AgNPs. Moreover, analysis of reactive oxygen species (ROS) generation and DNA damage indicated that TNFα-induced ROS-mediated DNA damage was reduced by 200 nm AgNPs, but not by 10 nm AgNPs. Tumor necrosis factor receptor 1 (TNFR1) was localized on the cell surface after TNFα exposure with or without 10 nm AgNPs. In contrast, the expression of TNFR1 on the cell surface was reduced by the 200 nm AgNPs. These results suggested that exposure of cells to 200 nm AgNPs reduces the TNFα-induced DNA damage response via reducing the surface expression of TNFR1, thus reducing the signal transduction of TNFα.

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