Objective To investigate the effect and mechanism of arsenic trioxide (As2O3) on the prevention of re steno sis after vascular injury. Methods Apoptosis induction of As2O3 on cultured rabbit vascular smooth muscle cells (VSMCs) in vitro was observed1 Thirty-two New Zealand white rabbits were randomly divided into 2-and 4-wk study groups, and their controls1 10%As2O3 at 215mg•Kg-1•d-1 or 0.9% sodium chloride was intraperitoneally infused for 3 days before left common carotid arteries were denudated with a balloon1 After denudation 2-and 4-wk animals were sacrificed for morphometry and immunohistochemical studies on carotid arteries, and for histopathology on liver and kidney. Results It was shown via cellular morphology and DNA fragments in electrophoresis that promotion of As2O3 on cultured vascular smooth muscle cell apoptosis was dependent upon its concentration and duration1 Compared with the control animals, the mean vascular intimal proliferation area s were reduced in 2-wk study animals (P<0.05) and no difference was shown in 4-wk (P>0.05), while the mean vascular luminal areas were all enlarged in both study groups (all P<0.05) 1 The downregulated bcl-2 expression (all P<0.05 in 2-and 4-wk) and the upregulatedbax expression (P<0.01 in 2-wk; P<0.05 in 4-wk) were detected by immunohistochemistry, in comparison with control group s1 Gene bcl-2 and baxprotein expression were consistent with the suppression of intimal proliferation and the enlargement of luminal areas in corresponding sections. Conclusion As2O3 induce s apoptosis of VSMCs and inhibit s experimental re steno sis effectively after artery injury, viadownregulation of bcl-2 and upregulation of baxexpre ssion.