Objective: To study the effects and mechanisms of protein kinase C(PKC) inhibitor(scutellarein) on cardiomyocyte apoptosis and ventricular remodeling in spontaneously hypertensive rats (SHR). Methods: 18 SHRs with left ventricular hypertrophy(LVH) aged 10 months were randomly divided into 3 groups and treated for 8 weeks with scutellarein

fosinopril and 0.9% sodium chloride solution(control) respectively.The effects of above drugs on systolic blood pressure (SBP)

heart rate (HR)

left ventricular hypertrophic index (left ventricular weight/body weight

LVW/BW)

cardiocyte ultramicrostructure

cardiac myocyte apoptosis

apoptosis-associated gene (Bax and Bcl-2 gene) protein expression and PKC activity were observed. Results: Compared with control group

scutellarein and fosinopril could significantly reduce left ventricular hypertrophic index(all P values less than 0.01)

ameliorate ultramicrostructure of cardiac hypertrophy

suppress Bcl-2 protein expression (all P values less than 0.01)

lower the membrane PKC (PKCm) activity(all P values less than 0.01)

stimulate Bax protein expression and promote cardiomyocyte apoptosis of SHRs with left ventricular hypertrophy (all P values less than 0.01). Fosinopril could remarkably decrease systolic blood pressure (all P values less than 0.01) but did not affect heart rate of SHRs with left ventricular hypertrophy (all P values more than 0.05). Scutellarein could not influence systolic blood pressure and heart rate of SHRs with left ventricular hypertrophy (all P values more than 0.05). Conclusion: Scutellarein and fosinopril can significantly reverse ventricular remodeling of SHR and preserve cardiac muscle. The mechanisms of their above-mentioned effects may be related to increase of cardiac myocyte apoptosis triggered by them via upregulation of apoptosis induced gene(Bax gene) expression and downregulation of apoptosis suppressor gene(Bcl-2 gene) expression as well as suppression of PKC activity.