Objective: To investigate the potential protective effects of Berberine(Ber) on doxorubicin(DOX)-induced myocardial cell injury and the underlying anti-oxidation mechanisms. Method: Rats with H9c2 cells were divided into:blank group

2μmol·L-1 DOX group

0.1μmol·L-1 Ber group

1μmol·L-1 Ber group

10μmol·L-1 Ber group

2μmol·L-1 DOX+0.1μmol·L-1 Ber group

2μmol·L-1 DOX+1μmol·L-1 Ber group

2μmol·L-1 DOX+10μmol·L-1 Ber group. Cell size and protein content were determined in various groups after different treatment time points. Expression of atrial natriuretic peptide(ANP) and brain natriuretic peptide(BNP) mRNA was detected by real-time PCR. Caspase-3 activity was used as the indicator to evaluate myocardial apoptosis level. DCFH fluorescent probe method was used to detect cellular ROS level

and at the same time determine malonaldehyde(MDA) in the cells

and evaluate oxidative damage level of myocardial cells. Result: Compared with blank group

the myocardial cell size and protein content in cells were increased in various treatment groups

with increase in ANP

BNP mRNA levels and enhancement of Caspase-3 activity

leading to cell apoptosis

decrease in intracellular ROS level

and has statistically significant differences(P<0.01). Conclusion: Ber protected H9c2 cells against the cardiotoxicity of DOX

and the reduction of oxygen free radicals in cardiac myocytes may be the underlying mechanism mediating the protective effect of Ber. Berberine reduces DOX-induced myocardial cell injury by antioxidant effect. Combination of Berberine and doxorubicin can inhibit DOX-induced myocardial hypertrophy

effectively reduce intracellular ROS level

remove lipid peroxides

and reverse DOX-induced myocardial cell apoptosis.