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H2 inhibits TNF-α-induced lectin-like oxidized LDL receptor-1 expression by inhibiting nuclear factor κB activation in endothelial cells.
- Source :
-
Biotechnology letters [Biotechnol Lett] 2011 Sep; Vol. 33 (9), pp. 1715-22. Date of Electronic Publication: 2011 May 05. - Publication Year :
- 2011
-
Abstract
- H(2) is a therapeutic antioxidant that can reduce oxidative stress. Oxidized low-density lipoprotein, which plays roles in atherosclerosis, may promote endothelial dysfunction by binding the cell-surface receptor LOX-1. LOX-1 expression can be upregulated by various stimuli, including TNF-α. Thus, we aimed to examine whether the upregulation of LOX-1 by different stimuli could be blocked by H(2) in endothelial cells. H(2) significantly abolished the upregulation of LOX-1 by different stimuli, including TNF-α, at the protein and mRNA levels. The TNF-α-induced upregulation of LOX-1 was also attenuated by the NF-κB inhibitor N-acetyl-L-cysteine. H(2) inhibited the TNF-α-induced activation of NF-κB and the phosphorylation of IκB-α. Furthermore, H(2) inhibited the expression of LOX-1 and the activation of NF-κB in apolipoprotein E knockout mice, an animal model of atherosclerosis. Thus, H(2) probably inhibits cytokine-induced LOX-1 gene expression by suppressing NF-κB activation.<br /> (© Springer Science+Business Media B.V. 2011)
- Subjects :
- Animals
Aorta pathology
Gene Expression drug effects
Humans
Immunohistochemistry
Male
Mice
NF-kappa B antagonists & inhibitors
RNA, Messenger biosynthesis
Receptors, Oxidized LDL antagonists & inhibitors
Tumor Necrosis Factor-alpha antagonists & inhibitors
Antioxidants metabolism
Endothelial Cells drug effects
Endothelial Cells metabolism
Hydrogen metabolism
NF-kappa B metabolism
Receptors, Oxidized LDL biosynthesis
Tumor Necrosis Factor-alpha metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1573-6776
- Volume :
- 33
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- Biotechnology letters
- Publication Type :
- Academic Journal
- Accession number :
- 21544615
- Full Text :
- https://doi.org/10.1007/s10529-011-0630-8