Selenoprotein S Attenuates Tumor Necrosis Factor-α-Induced Dysfunction in Endothelial Cells

Figure 8

Effect of SelS on the NF-κB pathway. Levels of nuclear NF-κB p65 in SelS plasmid (a) or SelS siRNA (b) transfected HUVECs after 10 ng/ml TNF-α treatment, determined by the western blot. The expression of cytoplasmic NF-κB p65 in HUVECs transfected with SelS plasmid (c) or SelS siRNA (d) and treated with 10 ng/ml TNF-α. Expression of IκBα (e) and phosphorylated IκBα (f) detected in different groups at indicated time points after 10 ng/ml TNF-α induction. Levels of IKKβ (g) and phosphorylated IKKβ (h) detected in HUVECs with different treatments after 10 ng/ml TNF-α induction. The cells were transfected with pcDNA3.1-SelS recombinant plasmid or SelS siRNAs for 30 h. The results are representative of triplicate independent experiments and are presented as mean ± SD, (). and versus control; versus empty vector at corresponding time point; and versus negative siRNA at corresponding time points. IκBα: inhibitory kappa B α; IKKβ: inhibitor of nuclear factor kappa-B kinase β; N-NF-κB p65: nuclear NF-κB p65; C-NF-κB p65: cytoplasmic NF-κB p65; E-vector: empty vector; Pc-SelS: pcDNA3.1-SelS plasmid; Neg.RNA: negative siRNA.

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