Objective Myocardial ischemia caused by coronary atherosclerotic cardiopathy is a serious disease that can cause death. This study describes the effects of ursolic acid on autophagy and apoptosis caused by serum deprivation of cardiomyocytes at the cellular level. Methods Rat H9c2 cardiomyocytes were cultured in vitro. The cells were divided into the control group, serum deprivation group, ursolic acid treatment group, autophagy inhibitor 3- methyladenine (3-MA) pretreatment combined with ursolic acid group, and rapamycin pretreatment combined with ursolic acid group. Apoptosis was detected using flow cytometry. Expression of the autophagy-related proteins LC3, Beclin1, and ATG5, and the apoptosis-related proteins cleaved-caspase3, BcL-2, and Bax, were detected by western blotting. Results 10 μM ursolic acid was the optimal concentration for H9c2 cells. Serum deprivation increased the expression of Beclin1 and ATG5 as well as the ratio of LC3II/ I in H9c2 cells (P< 0. 01), and these levels decreased after ursolic acid treatment (P< 0. 05). Serum deprivation caused an increase in the apoptosis rate of H9c2 cells (P< 0. 001), and ursolic acid treatment reduced the rate of apoptosis (P< 0. 01). The 3-MA pretreatment group had a further reduced apoptosis rate (P< 0. 001), while the rapamycin pretreatment group had an increased apoptosis rate (P< 0. 001). Serum deprivation increased the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 ( P < 0. 001). Following treatment with ursolic acid, the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 was decreased (P< 0. 01), and pretreatment with 3-MA further reduced the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 (P< 0. 001). The ratio of Bax / BcL-2 was increased in the rapamycin pretreatment group (P< 0. 05). Conclusions The anti-apoptotic effect of ursolic acid on serum-deprived H9c2 cells is related to the inhibition of autophagy.