Objective To discuss the expression of mitochondrial phosphate carrier (PiC) in myocardial injury caused by doxorubicin, and the protective mechanism of curcumin in myocardial injury caused by doxorubicin .Methods 60 adult SD rats were randomly divided into three groups:control group, doxorubicin group, curcumin+doxorubicin group.Control group was injected 0.9% sodium chloride injection (2.5 mL/kg) by rat tail vein injection, one times per week, 6 times in total.Doxorubicin group was injected with 0.5 mg/mL doxorubicin which diluted with 0.9% sodium chloride injection by rat tail vein injection, and the dosage was 1.25 mg/kg(about 0.5 mL).Curcumin+doxorubicin group was injected the same dose doxorubicin as doxorubicin group.After that, 12 mg/mL curcumin injection was added with 30mg/kg by rat tail vein injection.one times per week, 6 times in total.The glutathione peroxidase (Gpx) assay kit, superoxide dismutase (SOD) assay kit and malondialdehyde (MDA) detection kits were used to test the oxidative stress levels in myocardial cells of SD rats.Flow cytometry is used to test the SD rat cardiomyocytes transferred level. Application of Western blot and Real-time PCR technology were used to detect expression of PiC.ResuIts The Gpx activity and SOD vitality in myocardial cells of SD rats in curcumin with doxorubicin group all significantly increased compare with those of doxorubicin group, and all decreased compare with those of control group.But the rate of myocardial apoptosis, content of malondialdehyde and expression of Slc25a3 gene and PiC protein from myocardial cells of SD rats from curcumin with doxorubicin group all significantly increased compare with those of control group , and all decreased compare with those of doxorubicin group.ConcIusion Doxorubicin could increase the expression of PiC in myocardial mitochondria, the levels of oxidative stress, and the apoptosis of myocardial cells, and the effect of curcumin could be effective against the injury induced by doxorubicin .