Abstract:In this paper, the inhibition effect of curcumin/β-cyclodextrin polymer inclusion complex on the proliferation of HepG2 hepatocellular carcinoma cells was studied. MTT assay was used to investigate the effects of curcumin/β-cyclodextrin polymer inclusion complex with the different concentrations (40~640 μg/mL) and different periods of times (24 h, 48 h, and 72 h) on the cell viability of HepG2 cells. Then, the flow cytometry and measuring Caspase 3/8/9 activity were used to investigate the inhibiting mechanism of curcumin/β-cyclodextrin polymer inclusion complex on the proliferation of HepG2 cells. The results showed that with the increase in the treatment times and concentrations of curcumin/β-cyclodextrin polymer inclusion complex, the cell activity of HepG2 cells was gradually decreased. When the HepG2 cells were exposed to curcumin/β-cyclodextrin polymer inclusion complex (640 μg/mL) for 72 h, the cell activity reached the lowest as 9.81%±1.00%. Further flow cytometry analysis revealed that with the increase in the concentration of curcumin/β-cyclodextrin polymer inclusion complex, the number of apoptotic cells in HepG2 cells was gradually increased. When the cells were exposed to inclusion complex (640 μg/mL) for 72 h, the number of apoptotic cells (sub-G1) in HepG2 cells reached a maximum of 93.43%. The activity of Caspase 3/8/9 was also increased with the increasing concentration of curcumin/β-cyclodextrin polymer inclusion complex. The activity of caspase3/8/9 reached the maximum after the cells was exposed to inclusion complex (640 μg/mL) for 72 h. The results of western blot also showed that the protein expression level of Caspase 3/8/9 increased with the increase of the curcumin/β-cyclodextrin polymer inclusion complex concentration. The above results indicated that curcumin/β-cyclodextrin polymer inclusion complex inhibited HepG2 cells proliferation through mitochondrial pathways and death receptor pathways to induce HepG2 apoptosis.
