Inhibition of TNF-α induced ICAM-1, VCAM-1 and E-selectin expression by selenium

Zhang, Fan; Yu, Wei; Hargrove, James L.; Greenspan, Phillip; Dean, Roger G.; Taylor, Ethan Will; Hartle, Diane K.

doi:10.1016/s0021-9150(01)00672-4

Cited by 129 publications

(74 citation statements)

References 26 publications

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“…In this study, LgCL tended to decrease as the Se concentration increased in both men and women. One of the reasons for this may be the inhibition of inflammatory cytokines by Se that activates ROS production [32,33]. On the other hand, in women, LmCL showed a tendency to decrease as the serum Se concentration increased.…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between Serum Selenium Concentration and Neutrophil Function in Peripheral Blood

Lee

Takahashi

Matsuzaka

et al. 2011

Biol Trace Elem Res

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We evaluated the relationships between neutrophil-related functions and serum selenium (Se) concentration in the general population. We examined 800 subjects who had participated in the Iwaki Health Promotion Project in 2005 to determine the relationships between serum Se concentration and neutrophil-related functions such as the production capability of reactive oxygen species (ROS), phagocytic activity, and serum opsonic activity (SOA). In nonstimulated neutrophils, i.e., in neutrophils at their baseline condition before the application of the phagocytic stimulus, the serum Se concentration tends to be high and the ROS production tends to be low. With regard to SOA, there was a significant negative correlation between lucigenin-dependent chemiluminescence and serum Se concentration in both men and women. Moreover, in women, a significant negative correlation was observed between luminol-dependent chemiluminescence and serum Se concentration. These results suggest that subjects with a lower serum Se concentration may be exposed to a greater chronic oxidative stress due to neutrophil ROS production. In addition, the findings of our study suggest that women rather than men benefit more from Se against oxidative stress.

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Section: Discussionmentioning

confidence: 99%

The Relationship Between Serum Selenium Concentration and Neutrophil Function in Peripheral Blood

Lee

Takahashi

Matsuzaka

et al. 2011

Biol Trace Elem Res

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“…TNFα is a known inducer of adhesion molecules like vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1, which are required for monocyte adhesion to endothelial cells and subsequent tissue penetration, a process counteracted by selenium supplementation [16]. In addition, VCAM1 expression is decreased in cells overexpressing the selenoprotein GPx4 [17].…”

Section: Introductionmentioning

confidence: 99%

Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

Kipp

Banning

Schothorst

et al. 2012

The Journal of Nutritional Biochemistry

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Moderate selenium deficiency may lead to an impaired capacity to cope with health challenges. Functional effects of suboptimal selenium intake are not fully known, and biomarkers for an insufficient selenium supply are inadequate. We therefore fed mice diets of moderately deficient or adequate selenium intake for 6 weeks. Changes in global gene expression were monitored by microarray analysis in splenic leukocytes. Genes for four selenoproteins, Sepw1, Gpx1, Selh and Sep15, were the most significantly down-regulated in moderate selenium deficiency, and this was confirmed by quantitative polymerase chain reaction (qPCR). Classification of significantly affected genes revealed that processes related to inflammation, heme biosynthesis, DNA replication and transcription, cell cycle and transport were affected by selenium restriction. Down-regulation by moderate selenium deficiency of specific genes involved in inflammation and heme biosynthesis was confirmed by qPCR. Myeloperoxidase and lysozyme activities were decreased in selenium-restricted leukocytes, providing evidence for functional consequences. Genes for 31 nuclear factor (NF)-κB targets were down-regulated in moderate selenium deficiency, indicating an impaired NF-κB signaling. Together, the observed changes point to a disturbance in inflammatory response. The selenoproteins found here to be sensitive to selenium intake in murine leukocytes might also be useful as biomarkers for a moderate selenium deficiency in humans.

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“…The expression of COX-2 and TNF-a are synonymous with inflammation and are used as markers in many inflammatory diseases such as arthritis, atherosclerosis, and cancer [31]. Cyclooxygenase-2, TNF-α, and iNOS are inducible gene products considered to be bonafide markers of inflammation.…”

Section: Discussionmentioning

confidence: 99%

SeMet Mediates Anti-inflammation in LPS-Induced U937 Cells Targeting NF-κB Signaling Pathway

et al. 2014

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In previous studies, selenium (Se) was reported to play critical roles in anti-inflammatory activities. Nevertheless, limited information could be obtained during inflammation about selenomethionine (SeMet) in U937 human macrophage cells. The purpose of this study was to investigate the effects of SeMet on the inflammatory responses to lipopolysaccharide (LPS)-induced U937 macrophage cells and the signaling pathways targeted. U937 cells were pretreated with SeMet (1 μM) and subsequently induced with LPS (1 μg/ml) for 24 h. In the cell counting kit-8 assay (CCK-8), SeMet significantly inhibits the proliferation of U937 cells. SeMet also inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) stimulated by LPS. In the Western blot assay and real-time polymerase chain reaction (RT-PCR), SeMet significantly reduced protein expression and production of inducible NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α), and COX-2 in U937 cells. Furthermore, SeMet markedly suppressed the LPS-mediated activation of nuclear factor-kappa B (NF-κB) by blocking the degradation of inhibitor-κB proteins (IκBα) and lessening the translocations of P50 subunit content of NF-κB in the nucleus. These findings suggested the anti-inflammatory activity of SeMet in U937 cells; indicating that SeMet might be a potential treatment for inflammation therapy.

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Inhibition of TNF-α induced ICAM-1, VCAM-1 and E-selectin expression by selenium

Cited by 129 publications

References 26 publications

The Relationship Between Serum Selenium Concentration and Neutrophil Function in Peripheral Blood

The Relationship Between Serum Selenium Concentration and Neutrophil Function in Peripheral Blood

Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

SeMet Mediates Anti-inflammation in LPS-Induced U937 Cells Targeting NF-κB Signaling Pathway

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