| Objective:Investigate the influence of losartan on the expression of oxidized low-density lipoprotein (ox-LDL), induced in human monocytes-macrophages, tissue factor (TF) and its possible mechanism.Methods:In vitro density centrifugation the mononuclear cells of healthy people to develop and spread to the4th generation induced by phorbol ester (160nmol/ml) macrophages after24h culture used in the experiment. According to the experimental requirements are divided into blank control group, group of ox-LDL, LOX-1receptor blocker, poly inosinic acid group (Poly I), losartan group. By RT-PCR, measured in each group of LOX-1mRNA, the expression of TF mRNA, ELISA detection of TF protein expression status.Results:ox-LDL group and blank control group, the LOX-1mRNA and TF mRNA expression was significantly increased, a statistically significant difference (P<0.05). Poly inosinic acid (Poly â… ) of ox-LDL group of LOX-1mRNA and TF mRNA expression to reduce the TF expression was decreased, the difference was statistically significant (P<0.05). Losartan group and ox-LDL group of LOX-1mRNA and TF mRNA expression to reduce the TF expression was decreased, the difference was statistically significant (P<0.05).Conclusions:ox-LDL can induce human monocytes-macrophages of LOX-1mRNA. T F mRNA, TF expression was increased. LOX-1is the specificity of ox-LDL receptor, by ox-LDL through LOX-1may induce human monocyte-macrophage TF expression is in creased in macrophages in the atherosclerotic plaque over-expression of the TF to activat e exogenous coagulation pathway, leading to the occurrence of acute coronary syndrome (ACS). Losartan by down-regulating single-core-of LOX-1mRNA, macrophages, TF m RNA expression, thereby reducing the expression of TF, to reduce the formation of blood clots, reduce the incidence of acute coronary events. |