The Effect Of Curcrmin On The P53Protein Expression In HEPG2

Objective:The concept that cancer can be prevented or certain diet-derived substances can postpone its onset is currently eliciting considerable interest. Curcumin has been demonstrated to inhibit tumor initiation induced by various carcinogens. However, the molecular events of curcumin action have not been studied in detail. The aim of this paper was through the observation of curcumin on human liver cell HepG2P53protein expression level of influence, to explore the inhibit the growth of HepG2and inducing apoptosis effect and mechanism.Methods:Human liver cell HepG2were subcultured which were treated with the concentrations of curcumin at0μ mol/L、5μ mol/L、10μ mol/L、15μ mol/L、20μ mol/L、25μ mol/L、30μ mol/L、40μ mol/L and50μ mol/L. The effect of curcumin on proliferation of Human liver cell HepG2were detected by MTT method, IC50of curcumin were calculated according to the concentration of curcumin and Human liver cell HepG2inhibition ratio by regression analysis. The effect of curcumin on expression of wild type p53in tumor cells was detected by "Western blot method. The effect of curcumin on expression of Bax in Human liver cell HepG2was detected by Western blot method when the tumor cells were treated with PFT-a as the inhibitor of p53.Results:The proliferation of Human liver cell HepG2was inhibited by curcumin, and Human liver cell HepG2inhibition ratio was increased by the concentrations of curcumin increased. IC50of curcumin were calculated at19μ mol/L according to the concentration of curcumin and tumor cells inhibition ratio by regression analysis. Wild type p53in Human liver cell HepG2expression was very low without curcumin treatment, but was significantly higher in with the concentration of curcumin at30μ mol/L treatment (P<0.05). Bax in tumor cells expression was very low without curcumin treatment, but was significantly higher in with the concentration of curcumin at30μ mol/L treatment (P<0.05). Bax in tumor cells expression was very significant lower with curcumin and PFT-α mixture treatment than with curcumin treatment alone (P<0.05).Conclusion:1. Human liver cell HepG2proliferation was inhibited by curcumin in a dose dependent, and HepG2apoptosis was induced by curcumin.2. The amount of wild-type p53in Human liver cell HepG2was influenced by curcumin directly or indirectly.3. The expression of Bax was regulated by curcumin through p53.