ABSTRACT
AIM: To explore the molecular mechanisms of SC58125 on apoptosis in HepG2 cells. METHODS: Cell culture, ELISA, flow cytometry, RT-PCR, Western blot and electrophoretic mobility shift assay (EMSA) analysis were employed to clarify the effect of SC58125 on apoptosis in HepG2 cells and related molecular mechanisms. RESULTS: SC58125 induced apoptosis in HepG2 cells in a concentration-dependent manner, which was accompanied by inhibition of NF-?B, activation of caspase-3, decrease of bcl-2 mRNA and increase of p53 mRNA. However, no significant changes were found in the DNA binding of AP-1. CONCLUSION: SC58125 induces apoptosis in HepG2 cells, which may be related to the inhibition of NF-?B, activation of caspase-3, decrease of bcl-2 mRNA and increase of p53 mRNA.
ABSTRACT
AIM: To clarify the effect of SC58125 on cell proliferation and apoptosis in HepG-2 cells and explore the molecular mechanisms. METHODS: Cell culture, MTT, TUNEL, DNA ladder, flow cytometry and Western blot analysis were employed in the present study. RESULTS: SC58125 inhibited the growth of HepG-2 cells and induced the apoptosis. Furthermore, it arrested G_0/G_1 phase and inhibited S phase in HepG-2 cells. Depressed expression of P33 cdk2 ,P34 cdc2 ,cyclin B_1,cyclin E ,Mpm-2,Rb ,PCNA proteins were found in HepG-2 cells treated with SC58125. CONCLUSION: SC58125 inhibits cell proliferation and induces apoptosis, which may be related to the altered low protein levels of P33 cdk2 ,P34 cdc2 ,cyclin B_1,cyclin E ,Mpm-2,Rb,PCNA