The Effect Of Arsenic Trioxide On Endothelial Cells Proliferation And Nitric Oxide Production

Objectives: Several studies have suggested that arsenic trioxide (As2O3 ) can induce vascular smooth muscle cells apoptosis and inhibit restenosis after rabbit vascular injury. The vascular endothelium is an active, dynamic tissue that controls many important functions, including regulation of vascular tone and maintenance of blood circulation, fluidity, coagulation, and inflammatory responses. Injury of vascular after angioplasty can result restenosis . To keep the proliferation and restore the function of vascular endothelial cells are important of reducing restenosis. We investigated the effect of As2O3 on proliferation and nitric oxide (NO)release of endothelial cells, trying to evaluate its value of inhibiting restenosis.Methods: Human umbilical endothelial cells(ECV-304) wereincubated with As2O3 in vitro, and then the study was performed according to different As2O3 concentration groups : control group, 10μmol/L group, 5μmol/L group, 1μmol/L group, 0.5μmol/L group, 0.1μmol/L group,0.01μmol/L group , 0.001μmol/L group. MTT value, 3H-TdR incorporation and NO production were detected.Results: (1) As2O3 concentration of more than 0.1μmol/L caused injury of endothelial cells. (2) As2O3 more than 5μmol/L can inhibit endothelial cells incorporation of 3H-TdR, which indicated that As2O3 can inhibit the proliferation of endothelial cells. (3) NO production was reduced, when endothelial cells were incubated with As2O3 more than 0.5μmol/L .All the effects of As2O3 were dose-dependent and time-dependent.Conclusions: As2O3 of High concentration cause injury of endothelial cells. And As2O3 can inhibit the proliferation and nitric oxide production of endothelial cells. As2O3 of low concentration has no effect on endothelial cells.