And our results showed after FPKc and ES treatment for 24 h, the proportion of apoptotic cells increased obviously. Moreover, caspases which are a family of cysteine proteases play a central role during the process of apoptosis. Caspase-3, as one of the key executioners of apoptosis, is responsible for the proteolytic cleavage of many key proteins, such as the nuclear enzyme poly polymerase, which are cleaved in many different systems during apoptosis. Herein, our results showed cleaved-caspase 3 and cleaved-PARP were upregulated as the incubation time of FPKc and ES increased from 12 to 48 h. P53, as a tumor suppressor, could also induce apoptosis through targeting Bcl-2 family: up-regulating pro-apoptotic protein Bax and down-regulating anti-apoptotic protein Bcl-2. In the present study, our data showed that a decrease in Bcl-2 expression occurred accompanied with P53 expression increased in SW-480 cells which were treated with FPKc and ES. Thus we could conclude that FPKc induced apoptosis might belong to caspase dependent manner and P53 might also play an important role in this pro-apoptosis process. Previous studies indicate that the production of ROS is vertical in the pro-apoptosis effect of traditional Chinese medicine. Thus ROS generation was performed in this study. The results revealed that after incubation with FPKc and ES for 3 h and 6 h, the accumulation of cellular ROS was increased extremely, suggesting that ROS might be of great significance in FPKc induced apoptosis. Cellular GSH is capable of scavenging ROS and maintaining the redox state of cellular thiols. Depletion of cellular thiols may potentially lead to oxidative stress which means overproduction of ROS can be secondary to intracellular GSH depletion. What’s more, GSH may modulate the transcription of specific genes, VE-822 regulate redox-sensitive signal transduction and cell proliferation, apoptosis. Thus in our study, the concentration of intracellular GSH after FPKc and ES treating on SW-480 cells was performed. And the results showed GSH level was much lower than control after FPKc and ES treatment for 3 h and 5 h, which inferred FPKc induced the ROS accumulation through decreasing intracellular GSH content. Moreover, to further confirm the finding that the apoptotic effect of FPKc was mediated by ROS, antioxidants NAC was also employed. The results revealed NAC could decrease intracellular ROS generation, reverse DNA damage, relieved cell viability loss and apoptosis caused by FPKc treatment. These results indicated that ROS was involved in FPKc-induced apoptosis in SW-480 cells. Inhibition, the ability to suppress or resist irrelevant information, processes or responses, is a core function required for the control of thought and action. Changes in the efficiency of various cognitive abilities–from working memory to intelligence–have been attributed to the development or integrity of inhibitory control. Inhibition is often studied as resistance to interference and is commonly viewed as a family of related functions. However, there are differences in opinions on how the various functions are related or constituted.