50值分別為2.45及16.35 mmol/L,聯(lián)合用藥對(duì)細(xì)胞生長(zhǎng)抑制具有協(xié)同作用,Q值均大于1.15;聯(lián)合用藥能顯著降低細(xì)胞內(nèi)線粒體膜電位及p-mTOR蛋白表達(dá),顯著增加細(xì)胞內(nèi)活性氧產(chǎn)生及Cleave-Caspase3、p-AMPK蛋白表達(dá);抑制AMPK或mTOR能顯著增加聯(lián)合用藥對(duì)細(xì)胞的生長(zhǎng)抑制作用(P<0.05、0.01)。結(jié)論 2-DG聯(lián)合Met具有協(xié)同抑制HepG2細(xì)胞增殖作用,其機(jī)制與降低細(xì)胞線粒體膜電位,促進(jìn)活性氧產(chǎn)生、細(xì)胞凋亡,以及非AMPK依賴性的抑制mTOR活化有關(guān)。;Objective To investigate whether 2-deoxyglucose (2-DG) combined with metformin (Met) has synergistic antitumor effect on HepG2 cells, and explore the underling mechanisms. Methods The cell growth inhibitory ratio of HepG2 cells treated by 2-DG, Met, and the combination was determined by the resin azure method, and the synergistic antitumor effects of the combined application was also examined by calculating the Q values of Jin's formula; Mitochondrial membrane potential and reactive oxygen species generation were detected by high conformation cell imaging system; The expression level of Cleave-Caspase 3, p-AMPK, and p-mTOR were examined by Western blotting; The cell growth inhibitory ratio was detected by the resin azure method after AMPK and mTOR inhibitors administrating. Results The IC50 values of 2-DG and Met alone in HepG2 cells were 2.45 mmol/L and 16.35 mmol/L, respectively. Combined application has synergistic antitumor effects, and the Q values of Jin's formula was more than 1.15. Combined application significantly reduced mitochondrial membrane potential and increased intracellular reactive oxygen species production and Cleave-Caspase3 expression. Combined application significantly increased the expression of P-AMPK, decreased the expression of p-mTOR. Moreover, inhibiting AMPK and mTOR by the inhibitors significantly enhanced the cell growth inhibitory effect of combination group (P<0.05 and 0.01). Conclusion 2-DG combined with Met has synergistic antitumor effect on HepG2 cells. The underlying mechanism is related to decreasing mitochondrial membrane potential, promoting reactive oxygen production and apoptosis, and non-AMPK dependent inhibition of mTOR activation."/>