Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

Hsuan, Chin-Feng; Hsu, Hsia-Fen; Tseng, Wei‐Kung; Lee, Thung-Lip; Wei, Yufeng; Hsu, Kwan-Lih; Wu, Chau-Chung; Houng, Jer-Yiing

doi:10.3390/molecules200916908

Cited by 31 publications

(26 citation statements)

References 49 publications

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“…Irradiation causes elevation in TNF-a expression, which results in inflammation, apoptosis, and cell death by triggering NF-jB pathway. 15,16 Gamma irradiation (2 Gy) to the cells demonstrated a significant (P < 0.05) increase in TNF-a expression at 24 hours onwards as compared with unirradiated control cells ( Figure 5B), suggested activation of inflammatory response in the injured cells. However, NATG pre-treatment prior to irradiation was found to help in diminishing radiation-induced TNF-a expression at all tested time-points except 48 hours ( Figure 5B).…”

Section: Ifn-g Is Secreted From Macrophages and Activates Cytotoxic Tmentioning

confidence: 92%

“…that trigger inflammation and other cellular effects. [14][15][16] IL-10 has been identified as an immunosuppressive and anti-inflammatory cytokine secreted by monocytes, Th 2 cells, B cells, mast cells, dendritic and regulatory T cells, etc. [17][18][19] Upon irradiation, IL-10 expression has been found to be amplified, which affects antigen presentation capacity of APCs, resulting in inhibition of Th 1 cells activation in irradiated cells 20 resulting in immunosuppression.…”

Section: Introductionmentioning

confidence: 99%

“…Its mode of action includes activation of transcription factor NF‐κB and its downstream targets include COX‐2, IL‐1α, IL‐1β, IL‐6, etc. that trigger inflammation and other cellular effects . IL‐10 has been identified as an immunosuppressive and anti‐inflammatory cytokine secreted by monocytes, Th 2 cells, B cells, mast cells, dendritic and regulatory T cells, etc .…”

Section: Introductionmentioning

confidence: 99%

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In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

Malhotra

Singh

Kumar

2017

Environmental Toxicology

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Radiation-induced manifestations like free radical burst, oxidative damage and apoptosis leading to cell death. In present study, N-acetyl tryptophan glucopyranoside (NATG) was assessed for its immune-radioprotective activities using J774A.1 cells. Clonogenic cell survival, cell cycle progression and cytokines i.e. IFN-γ, TNF-α, IL-2, IL-10, IL-12, IL-13 and IL-17A expression were evaluated in irradiated and NATG pretreated cells using clonogenic formation ability, flow cytometry and ELISA assay. Results indicated that 0.25μg/ml NATG exhibited maximum radioprotection against gamma-radiation (2Gy) without intervening in cell cycle progression. NATG pretreated (-2 h) plus irradiated cells showed significant elevation in IFN-γ (∼38.2%), IL-17A (∼53.7%) and IL-12 (∼58.8%) expression as compared to only irradiated cells. Conversely, significant decrease in TNF-α (∼21.6%), IL-10 (∼31.2%), IL-2 (∼23.7%) and IL-13 expression (∼17.8%) were observed in NATG pretreated plus irradiated cells as compared to irradiated cells. Conclusively, NATG pretreatment to irradiated J774A.1 cells, stimulate Th while diminish Th cytokines that contributes to radioprotection.

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Section: Ifn-g Is Secreted From Macrophages and Activates Cytotoxic Tmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

Malhotra

Singh

Kumar

2017

Environmental Toxicology

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“…Then, the cells were pretreated with the MIF antagonist ISO-1 (25 μM) or rMIF (0.5 μg/mL) plus ISO-1 for 1 h. Next, the cells were infected with P. gingivalis ATCC 33277 at an MOI of 100 for 23 h. Next, 1 × 10 6 THP-1 cells were labelled with 5 μM calcein-AM and were co-cultured with the EA.hy926 cells for another 1 h. Non-adherent THP-1 cells were gently washed away with PBS twice. The adherent THP-1 cells remaining on the monolayer of endothelial cells were visualized using a fluorescence microscope (Nikon 80i, Tokyo, Japan); 3 fields under the microscope (× 100) were randomly selected; and the fluorescence-labeled THP-1 cells were assessed by cell counting assays [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Xu¹,

Pan²,

Xu³

et al. 2018

BMC Microbiol

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BackgroundPorphyromonas gingivalis (P. gingivalis), one of the main pathogenic bacteria involved in periodontitis, induces the expression of intercellular adhesion molecule − 1 (ICAM-1) and monocyte-endothelial cell adhesion. This effect plays a pivotal role in atherosclerosis development. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and critically affects atherosclerosis pathogenesis. In this study, we tested the involvement of MIF in the P. gingivalis ATCC 33277-enhanced adhesive properties of endothelial cells.ResultsEndothelial MIF expression was enhanced by P. gingivalis ATCC 33277 infection. The MIF inhibitor ISO-1 inhibited ICAM-1 production in endothelial cells, and monocyte-endothelial cell adhesion was induced by P. gingivalis ATCC 33277 infection. However, the addition of exogenous human recombinant MIF to P. gingivalis ATCC 33277-infected endothelial cells facilitated monocyte recruitment by promoting ICAM-1 expression in endothelial cells.ConclusionsThese experiments revealed that MIF in endothelial cells participates in the pro-atherosclerotic lesion formation caused by P. gingivalis ATCC 33277 infection. Our novel findings identify a more detailed pathological role of P. gingivalis ATCC 33277 in atherosclerosis.

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“…When the NF-κB signaling pathway is blocked, the expression of TNF-α and IL-6 is downregulated. 14 , 15 …”

Section: Introductionmentioning

confidence: 99%

Over-expression of nuclear factor-κB family genes and inflammatory molecules is related to chronic obstructive pulmonary disease

Zhou

Liu

Chen

et al. 2018

COPD

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BackgroundNuclear factor-κB (NF-κB) signaling plays essential roles in inflammatory responses. However, whether the expression levels of NF-κB family genes affect inflammatory responses is unclear. Moreover, little is known regarding the association between NF-κB family genes expression and the pathogenesis of chronic obstructive pulmonary disease (COPD). The present study was undertaken to assess the relationship between the expression levels of NF-κB family genes mRNA and of inflammatory markers relevant to COPD pathogenesis.MethodsA total of 186 unrelated patients with acute exacerbations of COPD and 180 healthy controls were recruited. Total RNA was extracted from the peripheral fasting blood of each subject using trizol reagent. The mRNA levels of NF-κB family genes (NF-κB1, NF-κB2 and c-REL) were measured by real-time quantitative polymerase chain reaction. The serum levels of cyclooxygenase-2 (COX-2), C-reactive protein, interleukin (IL)-1β, IL-6, IL-8, IL-12 and tumor necrosis factor-α were measured with enzyme-linked immunosorbent assay kits.ResultsThe relative mRNA levels of the NF-κB family genes and the levels of inflammatory molecules were significantly higher in the COPD group than in the control group after adjustment for smoking. The IL-1β, IL-8 and COX-2 levels were significantly lower in the NF-κB2 under-expression subgroup as compared to the NF-κB2 over-expression subgroup. The COX-2 level was significantly lower (P < 0.05) in the c-REL under-expression subgroup as compared to the c-REL over-expression subgroup.ConclusionNF-κB2 over-expression was associated with IL-1β, IL-8 and COX-2 levels, whereas c-REL overexpression was associated with COX-2 level. Over-expression of both NF-κB2 and c-REL was found to be related to COPD.

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Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

Cited by 31 publications

References 49 publications

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Over-expression of nuclear factor-κB family genes and inflammatory molecules is related to chronic obstructive pulmonary disease

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Glossogyne tenuifolia Extract Inhibits TNF-α-Induced Expression of Adhesion Molecules in Human Umbilical Vein Endothelial Cells via Blocking the NF-kB Signaling Pathway

Cited by 31 publications

References 49 publications

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

In vitro stimulatory effect of N‐acetyl tryptophan‐glucopyranoside against gamma radiation induced immunosuppression

Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor

Over-expression of nuclear factor-&kappa;B family genes and inflammatory molecules is related to chronic obstructive pulmonary disease

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Over-expression of nuclear factor-κB family genes and inflammatory molecules is related to chronic obstructive pulmonary disease