Objective To investigate the protective effect and mechanism of troxerutin ( TRX) on acutemyocardial toxicity induced by pirarubicin(THP) in rats. Methods THP was used to replicate acute myocardial toxicity inrats. Changes in cardiac weight, cardiac function, electrocardiogram, pathological morphology, and serum myocardialenzymes in the rats with acute myocardial toxicity induced by THP were observed. Western blot was used to determine theprotein levels of AKT, p-AKT, caspase-9, caspase-3, cleaved caspase-3, BCL-2 and BAX. Results TRX increased thecardiac coefficient of rats with acute myocardial toxicity induced by THP, improved their cardiac function, decreased thecontent of LDH, CK-MB, cTn-T and BNP, increased SOD and decreased the levels of MDA. TRX also activated AKT togenerate phosphoric acid. The levels of caspase-9, caspase-3 and BCL-2 were upregulated, and the levels of cleavedcaspase-3 and BAX were downregulated. Conclusions TRX attenuates acute myocardial toxicity induced by pirarubicin in rats by activating AKT and decreasing the expressions of related apoptotic proteins.