H2 inhibits TNF-α-induced lectin-like oxidized LDL receptor-1 expression by inhibiting nuclear factor κB activation in endothelial cells

Guohua Song, Hongle Zhang, Hua Tian, Jia Liu, Shu-Cun Qin, Xuejun Sun

Read more:

DOI: 10.1007/s10529-011-0630-8 DOI is the universal ID for this study.

This link will take you to the full study.


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.

Publish Year 2011
Country China
Rank Positive
Journal Biotechnology Letters
Primary Topic Heart
Secondary TopicAtherosclerosis
Model Mouse
Tertiary TopicLipid Metabolism
Vehicle Saline (Dissolved)
pH Neutral
Application Injection