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目的:探讨从白蔹抗肿瘤活性部位分离得到的没食子酸对人肝癌HepG2细胞生长的影响及其作用机制。方法:用不同浓度的没食子酸处理HepG2细胞,MTT法测定没食子酸对HepG2细胞生长增殖的抑制活性;采用Hochest染色、荧光显微镜、Annexin V-FITC/PI双标记法和流式细胞术观察凋亡细胞的形态结构变化以及定性、定量检测细胞凋亡;采用JC-1染色检测HepG2细胞线粒体膜电位变化情况。结果:没食子酸在12.5～200 mg·L-1对HepG2细胞生长有明显抑制作用,且呈一定的浓度依赖性;没食子酸能诱导HepG2细胞凋亡,降低细胞线粒体的膜电位。结论:没食子酸为白蔹抗肿瘤主要活性成分之一,通过降低细胞线粒体的膜电位而诱导细胞凋亡为其抗肿瘤作用机制之一。
Objective: To investigate the effect of gallic acid isolated from antitumor active site on the growth of human hepatocellular carcinoma HepG2 cells and its mechanism. Methods: HepG2 cells were treated with different concentrations of gallic acid. The inhibitory activity of gallic acid on the growth and proliferation of HepG2 cells was determined by MTT assay. Apoptosis was observed by Hochest staining, Annexin V-FITC / PI double labeling and flow cytometry Cell morphological changes as well as qualitative and quantitative detection of apoptosis; detection of JC-1 staining HepG2 cells mitochondrial membrane potential changes. Results: Gallicacid inhibited the growth of HepG2 cells at concentration of 12.5 ~ 200 mg · L-1, and showed a concentration-dependent manner. Gallic acid could induce the apoptosis of HepG2 cells and decrease the mitochondrial membrane potential. Conclusion: Gallic acid is one of the main anti-tumor active ingredients of Bletilla striata. Inducing apoptosis by reducing the membrane potential of mitochondria is one of its anti-tumor mechanisms.