Abstract:

Abstract:Objective To investigate the potential anti-atherosclerosis (AS) mechanism of lovastatin by  observing the influence of lovastatin on the  expressions of monocyte chemotactic protein-1 (MCP-1) and interleukin 10 (IL-10) in human umbilical vein endothelial cells (HUVECs) treated with tumor necrosis factor-α(TNF-α).Methods The HUVECs were routinely cultured in the medium RPMI 1640 containing 10% fetal bovine serum (FBS) in vitro and divided into 3 groups: control group,TNF-α  treated group (RPMI 1640 medium +TNF-α (20 μg/L),and lovastatin treated group (RPMI 1640 medium + 20 μg/L TNF-α+ 10 μmol/L Lovastatin);Application kit to detect ROS content; Real-time RT-PCR was used to measure the mRNA expressions of MCP-1 and IL-10 in HUVECs in each group;Western blotting method was used to analyze the protein expressions of MCP-1,NFκB and IL-10 in HUVECs in each group.Results Compared with the control group, the expressions of  ROS in TNF-α treated group were enhanced obviously(P<0.05).Compared with TNF-α treated group, the ROS expressions in the lovastatin treated group were decreased significantly(P<0.05).Compared  with  control group,the mRNA and protein expression levels  of MCP-1 and NFκB in TNF-α treated group were enhanced obviously (P<0.05),and the mRNA and protein expression levels  of IL-10 were decreased statistically (P<0.05).Compared with TNF-α treated group,the mRNA and protein expression levels  of MCP-1 and NFκB  in  lovastatin treated group were decreased significantly(P<0.05),but the expression level of IL-10 was increased statistically (P<0.05).Conclusion Lovastatin can inhibit the up-regulation of MCP-1 and NFκB and increase the expression of IL-10 in the HUVECs treated with TNF-α.Lavastatin may inhibit inflammation and prevent artherosclerosis through NF-κB pathway.

Key words: human umbilical vein endothelial cells, monocyte chemotactic protein-1, interleukin-10, atherosclerosis, lovastatin