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Selenium regulates transcription factor NF-kappaB activation during the acute phase reaction
Fusako Maehira1, Ikuko Miyagi, Yukinori Eguchi
1Laboratory of Clinical Biochemistry, Department of Health Technology, School of Health Sciences, University of the Ryukyus, Okinawa 903-0215, Japan. fmaehira@med.u.ryukyu.ac.jp
Summary
Selenium (Se) inhibits nuclear factor-kappaB (NF-kappaB) activation, reducing C-reactive protein (CRP) synthesis. Selenium deficiency promotes CRP production during inflammation.
Area of Science:
- Biochemistry
- Immunology
- Nutritional Science
Background:
- Observed inverse relationship between serum selenium (Se) and C-reactive protein (CRP) in various conditions.
- Investigated the role of Se in regulating nuclear factor (NF)-kappaB, a key factor in CRP synthesis.
Purpose of the Study:
- To determine the effect of selenium on NF-kappaB activation and subsequent C-reactive protein (CRP) synthesis.
- To clarify the implications of the reciprocal relationship between Se and CRP.
Main Methods:
- Used human hepatoma cell line (HuH-7) with Se deprivation and repletion.
- Stimulated cells with monocyte-conditioned medium (MoCM) or tumor necrosis factor-alpha (TNF-alpha).
- Assessed NF-kappaB activation via gel shift assay and CRP synthesis via ELISA.
Main Results:
- Physiological levels of Se inhibited NF-kappaB activation induced by MoCM and TNF-alpha.
- Maximal NF-kappaB activation and CRP synthesis occurred at Se concentrations found in pathological conditions with high CRP.
- These concentrations were approximately half the Se levels in healthy subjects.
Conclusions:
- Selenium at physiological levels inhibits NF-kappaB, a transcription factor regulating inflammatory cytokine genes.
- Reduced selenium levels induce hepatocyte synthesis of CRP during the acute phase response.