Inhibitory Effects Of Veratrum Nigrum L. Var.ussurience Nakai Alkaloids On The Hypertrophy Of Cardiomyocytes From Neonatal Rat

Objectives:Cardiac hypertrophy is not only an pathological change by many cardiovascular disease, also an independent risk factor for augmented mortalisty of cardiovascular diseases. Veratrum nigrum L.Var. ussurience Nakai alkaloids(VnA) is extracted from the root of Veratrum nigrum L.var.ussuriense Nakai, has been shown to decrease hypertension and thrombosis. The purpose of this project is to examine the effects of VnA on angiotensinⅡ(AngⅡ)-induced cardiomyocyte hypertrophy and to explore its possible mechanism.Methods:Cardiomyocytes isolated from neonatal Wistar rats were cultured in vitro and identified by immunocytochemistry(ICC). The cadiocytes were induced by AngⅡto set up myocardial hypertrophy model , Six groups were divided according to different treatments:①control group;②AngⅡgroup (10-7mol/L);③Cap group (2×10-4mol/L);④VnA group (0.001μg/L);⑤VnA group (0.003μg/L);⑥VnA group (0.009μg/L). The cell protein content, the cell diameter and the expressions of calcineurin(CaN) were measured respectively by BCA method, the micrometer and immunofluorescence analysis.Results:1. ICC confirmed that the purity of isolated cadiocytes is higher than 90%, indicating a good isolation of cadiocytes.2. AngⅡ(10-7mol/L) alone caused significant increases in the protein contents and diameters of cardiomyocytes. (P<0.01)3. Combination of VnA(0.003μg/L,0.009μg/L) and Captopril, inhibited significantly the increase in the protein content induced by AngⅡ. (P<0.01)4. Combination of VnA and Captopril, inhibited significantly the increase in the diameters induced by AngⅡ.(P<0.01)5. By immunofluorescence analysis, the expression of calcineurin(CaN) was obviously increased in the AngⅡ-induced model group. VnA decreased the expression of CaN significatly in a dose-dependent manner.Conclusions : VnA could inhibit the cardiomyocyte hypertrophy induced by AngⅡsignificantly and dose-depently. The possible mechanism may be related to the inhibition of CaN expression.