Chrysophanol‐induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential |
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| Authors: | Chien‐Hang Ni Chun‐Shu Yu Hsu‐Feng Lu Jai‐Sing Yang Hui‐Ying Huang Po‐Yuan Chen Shin‐Hwar Wu Siu‐Wan Ip Su‐Yin Chiang Jaung‐Geng Lin Jing‐Gung Chung |
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| Affiliation: | 1. Department of Chinese Medicine, E‐DA Hospital/I‐Shou University, , Kaohsiung 824, Taiwan;2. Graduate Institute of Chinese Medicine, China Medical University, , Taichung 404, Taiwan;3. School of Pharmacy, China Medical University, , Taichung 404, Taiwan;4. Department of Clinical Pathology, Cheng Hsin General Hospital, , Taipei 112, Taiwan;5. Department of Pharmacology, China Medical University, , Taichung 404, Taiwan;6. Department of Nutrition, China Medical University, , Taichung 404, Taiwan;7. Department of Biological Science and Technology, China Medical University, , Taichung 404, Taiwan;8. Graduate Institute of Clinical Medical Science, China Medical University, , Taichung 404, Taiwan;9. Division of Critical Care Medicine, Department of Internal Medicine, Changhua Christian Hospital, , Changhua 500, Taiwan;10. Department of Biotechnology, Asia University, , Taichung 413, Taiwan |
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| Abstract: | Chrysophanol (1,8‐dihydroxy‐3‐methylanthraquinone) is one of the anthraquinone compounds, and it has been shown to induce cell death in different types of cancer cells. The effects of chrysophanol on human lung cancer cell death have not been well studied. The purpose of this study is to examine chrysophanol‐induced cytotoxic effects and also to investigate such influences that involved apoptosis or necrosis in A549 human lung cancer cells in vitro. Our results indicated that chrysophanol decreased the viable A549 cells in a dose‐ and time‐dependent manner. Chrysophanol also promoted the release of reactive oxygen species (ROS) and Ca2+ and decreased the levels of mitochondria membrane potential (ΔΨm) and adenosine triphosphate in A549 cells. Furthermore, chrysophanol triggered DNA damage by using Comet assay and DAPI staining. Importantly, chrysophanol only stimulated the cytocheome c release, but it did not activate other apoptosis‐associated protein levels including caspase‐3, caspase‐8, Apaf‐1, and AIF. In conclusion, human lung cancer A549 cells treated with chrysophanol exhibited a cellular pattern associated with necrotic cell death and not apoptosis in vitro. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 740–749, 2014. |
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| Keywords: | chrysophanol necrosis human lung cancer A549 cells reactive oxygen species mitochondria membrane potential |
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