Effects and molecular mechanism of benserazide hydrochloride on LPS-induced inflammation in human umbilical vein endothelial cells

In this article, human umbilical vein endothelial cells(HUVECs)were induced by lipopolysaccharides(LPS)to establish an in vitro inflammation model to further verify the anti-inflammation effects of benserazide hydrochloride and to explore the molecular mechanisms involving in the anti-inflammation and anti-atherosclerosis of benserazide hydrochloride. The experiments were divided into blank groups(PBS+0. 5% FBS DMEM medium), model group ［LPS(500 μg/mL)+ 0. 5% FBS DMEM medium］ and drug group ［LPS(500 μg/mL)+benserazide hydrochloride+0. 5% FBS DMEM medium］. Western blot, ELISA and qPCR were used to detect the protein and mRNA expression levels of inflammatory cytokines SAP, TNF-α and MCP-1 in HUVECs cells. The expression levels of p65/p-p65, p38/p-p38, IκBα/p-IκBα, AKT/p-AKT and the nuclear translocations of p65, p38 and IκBα were detected by Western blot. The results showed that benserazide hydrochloride(1×10^-9, 1×10^-10, 1×10^-11 mol/L)could significantly inhibit the protein and mRNA expression of pro-inflammatory cytokines SAP, TNF-α and MCP-1. Besides, it could down-regulate the protein expression of p65/p-p65, p38/p-p38, IκBα/p-IκBα and AKT/p-AKT in the signal pathway while inhibiting the nuclear translocation of p65, p38 and IκBα, thereby inhibiting the transcriptional activity of the related genes.