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目的研究大黄素对人肝癌Huh7细胞的凋亡作用及分子机制。方法培养肝癌Huh7细胞,1、3、10、30、100μmol/L的大黄素处理24 h,5-氟尿嘧啶(5-FU)作为阳性药,MTT法检测细胞存活率;30μmol/L大黄素处理细胞0、3、6、24 h,光学显微镜观察细胞形态变化;Annexin V-FITC/PI双染法与流式细胞术检测细胞凋亡,Western blotting检测细胞凋亡相关蛋白的表达变化。结果大黄素显著抑制Huh7细胞生长且呈浓度依赖性,其IC50值为11.55μmol/L。30μmol/L大黄素处理细胞,随着药物作用时间的增加,细胞明显固缩和凝聚,大量细胞脱离培养皿底部;细胞凋亡明显;p-Akt、Bcl-2蛋白表达量减少,cleaved caspase-3蛋白表达量增加。结论大黄素通过Akt信号途径诱导肝癌Huh7细胞凋亡。
Aim To study the apoptosis of human hepatoma Huh7 cells induced by emodin and its molecular mechanism. Methods Huh7 cells were cultured and treated with 1,3, 10, 30 and 100 μmol / L of emodin for 24 h. 5-fluorouracil (5-FU) was used as positive drug. Cell viability was detected by MTT assay. 0, 3, 6 and 24 h respectively. The morphological changes of the cells were observed with light microscope. The apoptosis of the cells was detected by Annexin V-FITC / PI double staining and flow cytometry. The expressions of apoptosis related proteins were detected by Western blotting. Results Emodin significantly inhibited the growth of Huh7 cells in a concentration-dependent manner with an IC50 of 11.55 μmol / L. The cells were treated with 30μmol / L emodin, and the cells were obviously condensed and aggregated with the increase of drug action time. A large amount of cells detached from the bottom of the culture dish. The apoptosis of the cells was obvious. The expression of p-Akt and Bcl- 3 protein expression increased. Conclusion Emodin induces apoptosis of hepatocellular carcinoma Huh7 cells through Akt signaling pathway.