双去甲氧基姜黄素抑制肝癌细胞增殖并诱导凋亡的机制

Mechanism of bisdemethoxycurcumin inhabits proliferation of hepatocellular carcinoma cell and induces apoptosis

目的探讨双去甲氧基姜黄素(BDMC)对肝癌细胞的作用及其机制。方法不同BDMC(0、20、40、80μmol/L)干预肝癌细胞株HEPG2 72 h,MTT评价细胞增殖,Tunel分析细胞凋亡,ELISA检测活性氧(ROS)水平和p-STAT3水平,Western blot检测AMPK。采用ROS抑制剂N-乙酰-L半胱氨酸(NAC 2.5 mmol/L)处理30 min后BDMC再干预24 h,评价细胞凋亡能力。结果 BDMC可诱导肝癌细胞凋亡,增加ROS生成和AMPK磷酸化水平,抑制p-STAT3表达。抑制ROS生成可抑制BDMC诱导HEPG2凋亡的能力。结论 BDMC通过ROS/AMPK/STAT3信号通路诱导肝癌细胞凋亡。

Objective To investigate the effect and mechanism of bisdemethoxycurcumin （BDMC） on hepatocellular carcinoma cells. Methods Hepatoma cell line HEPG2 cells were treated with different concentrations of BDMC （0, 20, 40, 80 wmol/L） for 72 h, and then the cell prolifera- tion was measured by MTF. Cell apoptosis was evaluated by TUNEL analysis. ELISA was used to de- tect the level of intracellular reactive oxygen species （ROS） and STAT3 phosphorylation （ p-STAT3 ）, and Western blot was used to detect the expression of AMPK. Processed by ROS inhibitor N- acetyl -L cysteine （2.5 mmol/L NAC） for 30 min, cells were treated with BDMC for 24 h, and the ability of cell apoptosis was evaluated. Results BDMC was able to induce apoptosis of hepatocellular carcino- ma cells, increase the intracellular ROS production and AMPK phosphorylation levels, and inhibit the expression of p-STAT3 protein. Inhibition of ROS formation could effectively inhibit the ability of BD- MC in inducing apoptosis of HEPG2 cells. Conclusion BDMC induces apoptosis in hepatocellular carcinoma cells by ROS/AMPK/STAT3 signaling pathway.