Aim To observe the effect of rosiglitazone on apoptosis and expression of Phospho-Smad2/3 of thoracic aorta vascular smooth musle cell(VSMC)of hypercholesterol rat in vitro.Methods Primary cultures of rat VSMC were obtained enzymatically from dissociated hypercholesterol SD rat thoracic.Cells at passage five through eight were used in this experiment.After VSMC were serum-starved for 24 hours,they were randomly divided into two parts:part 1,cells were subdivided into four groups:①control group,②rosiglitazone group(concentration of rosiglitazone was 100umoll in this experiment),③rosiglitazone + GW9662 group,④rosiglitazone + anti-TGF-β1 group,the expression of p-Smad2/3 after 1 hour was detected by Western-blot.The apoptosis of VSMC was observed by flow cytometry after 24 hours;Part 2,cells were subdivided into two groups:①control group,②rosiglitazone group,expression level of p-Smad2/3 after 0,0.5,1,2,6,12,24 hours were detected by Western-blot.Results Our experiment show that the rate of apoptosis in VSMC treated with rosiglitazone was higher than control group(P<0.05)after 24 hours.The rate of apoptosis in VSMC in the groups treated with rosiglitazone + GW9662 or rosiglitazone + anti-TGF-β1 were higher than the group treated with rosiglitazone(P<0.05),from this we may conclude that GW9662 and anti-TGF-β1 would partly reverse the apoptosis of VSMC induced by rosiglitazone.The expression levels of p-Smad2/3 in the group treated with rosiglitazone were higher than the control group after 0.5 hour(P<0.05),and the expression level of p-Smad2/3 reached the highest in 1 hour(P<0.05)then decreased fast after top(P<0.05),from this we may conclude that rosiglitazone was able to induce VSMC expression p-Smad2/3.Furthermore,the levels of p-Smad2/3 in the group treated with rosiglitazone was higher than the groups treated with rosiglitazone + GW9662 or rosiglitazone + anti-TGF-β1,from this we may conclude that the GW9662 and anti-TGF-β1 both could partly reverse the expression levels of p-Smad2/3 in VSMC induced by rosiglitazone.Conclusion The apoptotic effect of rosiglitazone in VSMC would be mediated by a mechanism that includes the activation of PPAR-γ,inducing the apoptosis of VSMC by up-regulation of the expression level of the P-Smad2/3.