Objective To investigate the radiosensitization by curcumin on human laryngealcancer cell line Hep-2and it’s mechanism.Methods The human laryngeal cancer cell line Hep-2was treated with curcumin ofdifferent concentrations (100,50,25,20,12.5,6.25,0μmol/L) for24h,48h,72h respectiv-ely, joined DMSO or SDS, then the MTT assay was used to evaluate the cytotoxiceffects of curcumin on Hep-2cells and clonogenic assay was employed to observe theeffects on the radiosensitivity of the Hep-2. Combination paclitaxel of differentconcentrations (0.39,0.78,1.57μmol/L) with20μmol/L curcumin on Hep-2cells for24h.The flow cytometry was utilized to observe the apoptosis of Hep-2cells induced bycurcumin and the cell-cycle of Hep-2cells in response to X-ray irradiation.Results The curcumin could significantly inhibit the proliferation of Hep-2cells,with obvious dose-and time-dependent effects.The inhibit rate of cell growth of Hep-2cells after treated by curcumin with various concentrations had significantdifferences (P<0.05). The inhibit rate of cell growth of Hep-2cells after treatedby24h,48h,72h respectively had significant differences (P<0.05). The inhibit rate ofcell growth of Hep-2cells was under10%when treated by curcumin with20μmol/Lconcentrations and used it. When curcumin and paclitaxel were combined,theinductive effect on cell apoptosis became more obvious than the inhibit theproliferation of Hep-2cells with the paclitaxel only. Subtoxic dose of curcumin at20μmol/L could significantly reduce the clonogenic activity had significant differenceswith irradiation or curcumin (P<0.05). The apoptotic percentage of Hep-2cell linesexposed to free-medicine and with curcumin of20、25、50μmol/L respectively, was(2.68±1.07)%,(10.92±0.95)%,(18.87±2.34)%,(35.60±0.68)%respectively. Contrastthe team of exposed to free-medicine (2.68±1.07)%had significant differences(P<0.05). Irradiation or curcumin resulted in cell cycle arrest at G2/M phase in Hep-2cells. Conclusion Curcumin can enhance the radiosensitivity of the human laryngealcancer cell line Hep-2in vitro.The mechanism may involve the increased apoptosisand prolonged cell cycle arrest induced by the combined treatment.The combinationof curcumin and paclitaxel enhanced the effect and put down the toxieation inchemotherapy.... |