Objective    To investigate the role of PI3K/AKT and ERK1/2 signaling pathways in the process of cardiomyopathy induced by doxorubicin (DOX).     Methods    Twenty SD rats were divided into two groups: DOX group (10 rats that were injected through caudal vein with 2.5 mg/kg DOX

once a week

for 6 weeks) and control group (10 rats). At 5

th

week after the end of DOX injection

the structural changes and functional damage were examined

and the apoptosis rate of cardiomyocytes and the expression levels of p-AKT and p-ERK1/2 were determined.     Results    Eleven weeks after the DOX injection

the myocardial pathological changes were mainly myofibrillar loss and cytoplasmic vacuolization. DOX could induce compensated heart function (the value

of FS% was 34

P0.01 as compared with control group). DOX caused cardiac cell apoptosis and the apoptosis ratio was 28.4% (P0.01

as compared with control group). The expression of Bcl-2 increased to 126% (P0.05) and Bax to 338% (P0.05) of control level. In DOX group

phosphorylation of Akt was reduced to 12% (P0.05) and that of ERK1/2 was reduced to 24% (P0.05) of control level.     Conclusion    DOX can induce the damage of cardiac function and the apoptosis of cardiomyocytes

in which the PI3K/AKT and ERK1/2 signaling pathways may play important roles.