In this study, the GSPs-treated HeLa and SiHa cells were found to express significantly less Bcl-2 protein and more Bak-1 protein than the untreated cells, suggesting that both Bcl-2 and Bak-1 play roles in GSPs-induced apoptosis in cervical cancer cells. It was reported that the activation of Bak-1 could disrupt the normal function of Bcl-2 and lead to the loss of mitochondrial membrane potential and enhancement of mitochondrial membrane permeability, which in turn Idalopirdine hydrochloride result in the release of Cytochrome c and apoptosisinducing factors from mitochondria into the cytosol. Subsequently, cytosolic Cytochrome c, Apaf-1 and ATP form the apoptosome complex, which activates pro-caspase-9, finally leading to the activation of caspase-3, one of the key mediators of apoptosis, followed by cell death. In the present study, the treatment of HeLa and SiHa cells with GSPs resulted in a significant loss of mitochondrial membrane potential and increased activity of caspase-3. Moreover, TUNEL assays and caspase-3 detection revealed that the tumor xenograft tissues from the GSPs-treated group contained more apoptotic cells and greater caspase-3 activity than the control. All these results suggested that GSPs induced the apoptosis of cervical cancer cells Xylose through the mitochondrial pathway. To determine whether GSPs also exert an inhibitory effect on cervical cancer in vivo, tumor xenograft experiments with HeLa and SiHa cells were performed on nude mice fed GSPs-containing water. The results showed that GSPs administration remarkably inhibited the initiation and progression of tumor xenografts. Additionally, the GSPs treatment also inhibited tumor growth even if the tumor xenografts had been established, suggesting that GSPs have the potential to be used not only as a preventive drug but also as a therapeutic treatment for cervical cancer. In summary, our studies demonstrated the anticancer efficacy of GSPs through the induction of apoptosis in cervical cancer cells in vitro and in vivo.Based on our results and other previous research, we speculated that GSPs could trigger the apoptosis of cervical cancer cells through the mitochondrial pathway, characterized by Bcl-2 down-regulation, Bak-1 up-regulation, the loss of mitochondrial membrane potential and the increased activity of caspase-3.