辣椒素通过氧化应激诱导HepG2肝癌细胞凋亡的研究

Capsaicin Induces Apoptosis in HepG2 Cells Through ROS Activation

[目的]观察辣椒素对HepG2细胞增殖和凋亡的影响及其分子机制。[方法]采用CCK8法观察辣椒素对HepG2细胞增殖的影响,流式细胞术和JC-1探针检测辣椒素对HepG2细胞凋亡率和线粒体膜电位的影响,采用DCFH-DA探针联合高内涵分析仪检测氧化应激表达水平的变化。[结果]辣椒素可剂量依赖性抑制HepG2细胞增殖、诱导细胞凋亡。200μmol/L辣椒素作用24h可引起HepG2细胞明显坏死、脱落和漂浮。相比对照组,200μmol/L辣椒素明显降低HepG2细胞线粒体膜电位红绿荧光表达量比值（8.39±0.12 vs 4.23±0.04）。200μmol/L辣椒素可引起HepG2细胞内氧化应激水平上调1.78倍。使用还原剂维生素C抗氧化可恢复细胞活力,减轻凋亡。[结论]辣椒素剂量依赖性诱导人肝癌HepG2细胞凋亡,其机制与氧化应激水平过激活相关。

[Purpose] To investigate the effects of capsaicin on the proliferation and apoptosis of HepG2 cells. [Methods] Human liver cancer HepG2 cells were treated with 200μmol/L capsaicin for 12 h or 24 h. The cell proliferation was assessed with cell counting kit-8（CCK-8）;cell apoptosis was detected with flow cytometry;mitochondrial membrane potential changes were determined by JC-1 probe staining;the oxidative stress was determined by DCFH-DA probe in combination with high-throughput screening（HTS） applications. [Results] Capsaicin showed anti-proliferative and pro-apoptotic effects on HepG2 cells in a dose-dependent manner（P〈0.01）. Compared with untreated cells,the mitochondrial membrane potential in HepG2 cells was decreased after treatment of200μmol/L capsaicin for 24 h（8.39 ±0.12 vs 4.23 ±0.04,P 〈0.01）.The level of reactive oxygen species（ROS） in HepG2 cells was increased by 1.78 times after capsaicin treatment. The capsaicininduced cell damage and apoptosis were alleviated by pretreatment of antioxidant Vitamin C.[Conclusion] Capsaicin induces apoptosis in human liver cancer HepG2 cells through the activation of reactive oxygen species.