白蔹药效成分没食子酸抑制人肝癌HepG2细胞生长及作用机制研究

HepG2 Proliferation Restriction and Active Mechanis of Gallic Acid as Active Compound in Ampelopsis japonica

摘要:

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。

Abstract:

Objective:To discuss the effects and active mechanism of gallic acid (GA) as main active compound in Ampelopsis japonica (AJ) to HepG2 cells proliferation. Method: The MTT method was used to determine restriction activity of GA to HepG2 cells proliferation after HepG2 cells were treated with different GA concentration. Hoechst dyeing method, fluorescence microscope, annexin V-FITC/PI double-labeling method and flow cytometry method were used to observe morphological structure change of apoptotic cells and to detect cell apoptosis quantitatively and qualitatively. Finally, JC-1 dyeing method was used to detect the potential change of HepG2 cells mitochondrial membrane. Result: The restriction of GA to HepG2 proliferation is effective in concentration of 12.5-200 mg·L^-1. GA is concentration-dependence, and has an ability of inducing HepG2 cells apoptosis and reducing potential of mitochondria. Conclusion: GA is one of principle anti-tumor constitutes of AJ. And one of its anti-tumor mechanism is inducing cell apoptosis by reducing potential change of mitochondria.