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The role of reactive oxygen species in the apoptotic effects of curcumin and simvastatin on lung cancer cell line
Author(s) -
Lee Sang Haak,
Kim In Kyoung,
Lee Hye In,
Lee Hwa Young,
Ban Woo Ho,
Kim Sei Won,
Kang Hyeon Hui,
Moon Hwa Sik
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1105.20
Subject(s) - curcumin , simvastatin , apoptosis , reactive oxygen species , chemistry , pharmacology , intracellular , cancer cell , viability assay , cell growth , cancer research , cancer , biochemistry , biology , medicine
Curcumin is known to have anti‐inflammatory properties and induce apoptosis of cancer cells. The statins have been proven as effective anticancer agents through inhibition of cell proliferation and induction of apoptosis. However, the precise molecular anticancer mechanisms and synergic effects of these agents have not been elucidated in lung cancer cells. Curcumin and simvastatin caused morphologic changes in A549 cells and inhibited the growth of the cell in a concentration dependent manner, especially the synergistic inhibition of cell proliferation with simvastatin (1 uM) and curcumin (20 uM). Curcumin promoted the expression of apoptosis related genes such as active caspase‐3, 9, p53 and p21 after 24 hrs. Intracellular reactive oxygen species (ROS) were significantly increased after treatment with curcumin and simvastatin up to 24 hrs in a dose dependent manner. Cells were treated with antioxidant N‐acetyl‐L‐cystein (NAC) before the simvastatin and curcumin, and the results showed that NAC decreased the intracellular ROS level and reversed the decreased cellular viability induced by the agents. Our data indicates that combination of curcumin and simvastatin has synergistic anti‐proliferative effects. Therefore, we suggest that curcumin and simvastatin may have anticancer and potential chemopreventive actions through ROS‐mediated apoptosis pathway.