ApoM Suppresses TNF-alpha-Induced Expression of ICAM-1 and VCAM-1 Through Inhibiting the Activity of NF-kappa B

摘要

To explore the anti-inflammatory effect of apolipoprotein M (apoM) on regulation of tumor necrosis factor- (TNF-)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and further investigate the molecular mechanism of apoM in this process. We found that TNF- could decrease expression of apoM and inhibitor of NF-B- (IB) in HepG2 cells. Overexpression of apoM caused a significant decrease of ICAM-1 and VCAM-1 expression, while it caused a significant increase of IB expression in HepG2 cells. Furthermore, the treatment with TNF- could increase ICAM-1 and VCAM-1 expression, decrease IB protein expression, and increase nuclear factor-B (NF-B) activity, and these effects were markedly enhanced by small interfering RNA (siRNA)-mediated silencing of apoM in HepG2 cells. Our findings demonstrated that apoM suppressed TNF--induced expression of ICAM-1 and VCAM-1 through inhibiting the activity of NF-kappa B.