Objective To examine the effects of Veratrum nigrum L.Var.ussurience Nakai alkaloids(VnA)on angiotensin Ⅱ(AngⅡ)-induced cardiomyocyte hypertrophy and to explore its possible mechanism.Methods The cadiocytes were induced by AngⅡ to set up myocardial hypertrophy model,the animals were divided into six groups according to the different treatments:control group,model group,positive control group,VnA group(low,middle and high dose).The cell protein content,the cell diameter and the expression of calcineurin(CaN)were measured respectively by BCA method,the micrometer and immunofluorescence analysis.Results VnA(middle and high dose)and Captopril inhibited significantly the increase in the protein content induced by AngⅡ(P<0.01).VnA and Captopril inhibited significantly the increase in the diameters induced by AngⅡ(P<0.01).By immunofluorescence analysis,the expression of calcineurin(CaN)was obviously increased in the AngⅡ-induced model group.VnA decreased the expression of CaN significantly.Conclusions VnA could inhibit the cardiomyocyte hypertrophy induced by AngⅡ significantly in a dose-dependent manner.The possible mechanism may be related to the inhibition of CaN expression. Objective To examine the effects of Veratrum nigrum L.Var.ussurience Nakai alkaloids(VnA) on angiotensin II(AngII)-induced cardiomyocyte hypertrophy and to explore its possible mechanism.Methods The cadiocytes were induced by AngII to set up myhypertrophy model,the The animals were divided into six groups according to the different treatments:control group,model group,positive control group,VnA group(low,middle and high dose).The cell protein content,the cell diameter and the expression of calcineurin(CaN)were Bounding by BCA method, the micrometer and immunofluorescence analysis.Results VnA (middle and high dose) and Captopril inhibited significantly increase the protein content induced by AngII (P<0.01). VnA and Captopril inhibited significant increase in the diameters induced By AngII(P<0.01).By immunofluorescence analysis,the expression of calcineurin(CaN)was significantly increased in the AngII-induced model group.VnA decreased the expression of CaN sign ificantly.Conclusions VnA could inhibit the cardiomyocyte hypertrophy induced by AngII significantly in a dose-dependent manner. The possible mechanism may be related to the inhibition of CaN expression.