Plant Resources Research Institute, Duksung Women's University, Seoul 132-714, South Korea.
Chin J Cancer Res. 2013 Oct;25(5):536-43. doi: 10.3978/j.issn.1000-9604.2013.10.02.
The aim of the present study was to investigate antioxidant and the anticancerigen activity of a methanol extract from Artemisia princeps var. orientalis (APME), a well-known traditional herbal medicine in Asia, in hepatocellular cancer cells.
To evaluate the antioxidant activity of APME, reactive oxygen species (ROS) and the antioxidant enzymes, superoxide dismutase (SOD) and catalase were investigated in HepG2 cells exposed to APME (5, 100, and 200 µg/mL) for 72 h. Then, to evaluate the anticancer activity of APME, we investigated the proliferation and apoptosis induction of HepG2 and Hep3B cells exposed to APME (1-200 µg/mL) for 24, 48, and 72 h.
APME dose-dependently reduced the generation of ROS in the presence of H2O2 compared with control cells. Furthermore, it increased catalase and SOD activity. Moreover, APME inhibited cell proliferation in a dose- and time-dependent manner, but at concentrations lower than 100 µg/mL, the inhibition was less dose-dependent than time-dependent. HepG2 and Hep3B cells exposed to 5, 100, and 200 µg/mL APME for 72 h underwent cell cycle arrest and apoptosis. Exposure to APME resulted in a significant increase in the number of cells in G1 phase and a decrease in the G2/M phase cell population. In addition, APME induced P53 expression of HepG2 cells in a dose-dependent manner, and played a role in the downregulation of Bcl-2 and upregulation of Bax in both HepG2 and Hep3B cells.
These results indicate the potential role of APME as an antioxidant and anticancerigen agent in hepatocarcinoma cell lines.
本研究旨在探讨亚洲著名传统草药黄花蒿甲醇提取物（APME）对肝癌细胞的抗氧化和抗癌活性。
为了评估 APME 的抗氧化活性，我们在 HepG2 细胞中研究了 APME（5、100 和 200μg/ml）暴露 72 小时后活性氧（ROS）和抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶的变化。然后，为了评估 APME 的抗癌活性，我们研究了 HepG2 和 Hep3B 细胞暴露于 APME（1-200μg/ml）24、48 和 72 小时后的增殖和凋亡诱导作用。
APME 可剂量依赖性地降低 H2O2 存在时 ROS 的产生，与对照细胞相比。此外，它增加了过氧化氢酶和 SOD 的活性。此外，APME 呈剂量和时间依赖性抑制细胞增殖，但在低于 100μg/ml 的浓度下，抑制作用的剂量依赖性小于时间依赖性。暴露于 5、100 和 200μg/ml APME 的 HepG2 和 Hep3B 细胞经历细胞周期停滞和凋亡。APME 暴露导致 G1 期细胞数量显著增加，G2/M 期细胞群减少。此外，APME 以剂量依赖性方式诱导 HepG2 细胞中 P53 的表达，并在 HepG2 和 Hep3B 细胞中下调 Bcl-2 和上调 Bax。
这些结果表明 APME 作为一种抗氧化和抗癌剂在肝癌细胞系中具有潜在作用。
