Antioxidant and anticancer activity of Artemisia princeps var. orientalis extract in HepG2 and Hep3B hepatocellular carcinoma cells
Antioxidant and anticancer activity of Artemisia princeps var. orientalis extract in HepG2 and Hep3B hepatocellular carcinoma cells
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DOI：
10.3978/j.issn.1000-9604.2013.10.02
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发表时间：
2013-10-01
影响因子：
5.1
通讯作者：
Kim, Gun-Hee
中科院分区：
文献类型：
--
作者：
Choi, Eun-Jeong;Kim, Gun-Hee
目的：研究青蒿醇提物的抗氧化和抗癌活性。方法：观察不同浓度(5、100、200 mU g/mLAPME)作用于人肝癌细胞72 h后对肝癌细胞的抗氧化活性、抗氧化酶、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性的影响，并观察APME(1~200 mU g/mLAPME)对肝癌细胞增殖和凋亡的影响。结果：与对照组细胞相比，APME可剂量依赖性地减少过氧化氢存在下细胞内ROS的产生。此外，还能提高过氧化氢酶和超氧化物歧化酶的活性。此外，APME以剂量和时间依赖的方式抑制细胞增殖，但当浓度低于100微克/毫升时，抑制作用不是剂量依赖而是时间依赖。5、100和200mUg/mLAPME作用于HepG2和Hep3B细胞72h后，细胞周期受阻，细胞发生凋亡。经APME处理后，G1期细胞明显增多，G2/M期细胞明显减少。此外，APME还以剂量依赖的方式诱导HepG2细胞P53的表达，并在两种细胞中发挥下调Bcl2和上调Bax的作用。结论：APME作为一种潜在的抗氧化剂和抗癌原剂对肝癌细胞具有潜在的作用。
Objective: 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.Methods: 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 mu g/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 mu g/mL) for 24, 48, and 72 h.Results: 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 mu g/mL, the inhibition was less dose-dependent than time-dependent. HepG2 and Hep3B cells exposed to 5, 100, and 200 mu g/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.Conclusions: These results indicate the potential role of APME as an antioxidant and anticancerigen agent in hepatocarcinoma cell lines.