Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

Sodium tanshinone IIA sulfonate (STS), a water-soluble derivative of tanshinone IIA, has been demonstrated to have potent anti-inflammatory properties. However, the protective effects of STS on lipopolysaccharide (LPS)-induced inflammation in endothelial cells remain to be elucidated. In the present study, human umbilical vein endothelial cells (HUVECs) were used to explore the effects of STS on LPS-induced inflammation and the molecular mechanism involved. HUVECs were pretreated with STS for 2 h, followed by stimulation with LPS. Then expression and secretion of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta, and the activation of nuclear factor-kappa B (NF-kappa B) were assessed. The results demonstrated that STS significantly decreased LPS-induced TNF-beta and IL-1 beta protein expression in HUVECs. Similarly, the increased levels of TNF-alpha and IL-1 beta in cell supernatants stimulated by LPS were also significantly inhibited by STS. Furthermore, STS inhibited LPS-induced NF-kappa B p65 phosphorylation and nuclear translocation. All the results suggest that STS prevents LPS-induced inflammation through suppressing NF-kappa B signaling pathway in endothelial cells, indicating the potential utility of STS for the treatment of inflammatory diseases.