Study on the protective effects of taxifolin on human umbilical vein endothelial cells and THP-1 cells damaged by hexavalent chromium: A probable mechanism on preventing cardiovascular disease induced by heavy metal

Hexavalent chromium [Cr(VI)] is a kind of heavy metal with strong oxidizing ability, which can induce cardiovascular disease (CVD), while taxifolin can protect cells and organisms suffering oxidative stress. In this study, the inhibitory effects of taxifolin against Cr(VI)-induced cells damage in human umbilical vein endothelial cells (HUVECs) and THP-1 cells were investigated. Cr(VI) could increase the phosphorylation of p-38 and JNK, upregulate the ratio of Bax/Bcl-2 in the both cell lines. Meanwhile, the Cr(VI) stimulation led to an increase in the expression of ICAM-1, VCAM-1 and upregulated adhesion of THP-1 cells to HUVECs. Furthermore, Cr(VI) could induce the activation of the nuclear factor kappa B (NF-κB) signaling pathway, the accumulation of p65 in the nucleus, and the increase in the phosphorylation of IκB and the expression of Cleaved-Caspase-1 and IL-1β in THP-1 cells. However, taxifolin could reverse the effects by inhibiting the activation of mitogen-activated protein kinases (MAPKs) and NF-κB signaling pathways, regulating the expression of apoptosis-related proteins, and alleviating the adhesion of THP-1 cells to HUVECs. Our findings demonstrated that taxifolin was a potential agent to prevent endothelial dysfunction, monocyte inflammation and cell adhesion induced by Cr(VI).