Objective To investigate the protective effect of FUC on adriamycin (ADR) - induced myocardial cell toxicity. Methods Using DPPH FUC method to study the scavenging effect on free radicals play a protective role of H9C2, MTT method is used to study the cytotoxicity of FUC on ADR induced by the H9C2 cell morphological changes were observed by AO/EB staining, the expression of H9C2 in cells of ROS levels and H9C2 cell apoptosis related protein Carboxy-DCFDA Western and Blotting detection method. Results DPPH assay showed that FUC has strong scavenging of oxygen free radicals, FUC to play a good protective effect H9C2 cytotoxicity caused by ADR and mechanism of apoptosis in H9C2 cells were cytotoxic FUC protective effect of H9C2 on ADR induced by the reduced ADR induced increase, elevated levels of reactive oxygen species that caused by ADR the H9C2 cells and H9C2 cells apoptosis protein Caspase-8 Cleaved Cas-pase-3, Cleaved and downreguLation of PARP upreguLation inhibited. Conclusion The protective effect of FUC on myocardial cell toxicity caused by ADR is played by oxidative stress in myocardial cells by antioxidant activity has its own ADR induced inhibition of blocked ADR induced myocardial cell activation of Caspase-8 pathway, thereby effectively inhibit ADR induced Cas-pase-3 activation and PARP shear this continuous process to achieve.