Objective:To investigate the apoptosis-inducing effect of baohuoside I (BI) on endometrial cancer Ishikawa cells and its related molecular mechanism.Methods:With 0 μ M and 0 h treatment were used as blank control group, and BI treatment was used as experimental group. The inhibitory effect of BI on the proliferation of Ishikawa cells was detected by CCK-8 assay. The apoptosis-inducing effect of BI on Ishikawa cells and the changes of mitochondrial membrane potential were detected by flow cytometry. The expressions of apoptosis-related proteins and signaling pathway-related proteins were detected by Western blot.Results:CCK-8 experiment showed that BI could be expressed in concentration gradient (3, 10, 20, 30, 40 μM). It could effectively inhibit the proliferation of Ishikawa cells (the survival rates were 89.56±0.96, 74.69±1.21, 60.28±1.09 and 43.51±2.17 respectively). Its toxic and side effects on normal cells were lower than that of 5-FU. The results of flow cytometry showed that BI could effectively induce the apoptosis of Ishikawa cells by reducing the level of mitochondrial membrane potential. The proportion of apoptotic cells in each group was (9.92±0.77) %, (14.01±0.83) %, (17.05±1.41) %, (28.21±1.73) % and (44.55±3.11) %. Western blot showed that BI could up-regulate the level of p-p38 and reduce the level of p-STAT3.Conclusions:BI can effectively inhibit the proliferation of Ishikawa cells, and induce apoptosis by reducing the mitochondrial membrane potential and activating the mitochondria-dependent pathway. Its regulatory mechanism is achieved by activating the p38 signaling pathway and inhibiting the STAT3 pathway.