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Evidence-Based Complementary and Alternative Medicine
Volume 2011, Article ID 523596, 13 pages
Research Article

Emodin Induces Apoptotic Death in Murine Myelomonocytic Leukemia WEHI-3 Cells In Vitro and Enhances Phagocytosis in Leukemia Mice In Vivo

1School of Chinese Medicine, China Medical University, Taichung 404, Taiwan
2School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 404, Taiwan
3Department of Chinese Medicine and Chinese Internal Medicine, China Medical University Hospital, Taichung 404, Taiwan
4School of Pharmacy, China Medical University, Taichung 404, Taiwan
5Department of Pharmacology, China Medical University, Taichung 404, Taiwan
6Department of Health and Nutrition Biotechnology, Asia University, Taichung 412, Taiwan
7Department of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan
8Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan
9Department of Food and Beverage Management, Technology and Science Institute of Northern Taiwan, Taipei 112, Taiwan
10Department of Biotechnology, Asia University, Taichung 412, Taiwan

Received 6 January 2011; Revised 28 February 2011; Accepted 3 March 2011

Copyright © 2011 Yuan-Chang Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Emodin is one of major compounds in rhubarb (Rheum palmatum L.), a plant used as herbal medicine in Chinese population. Although many reports have shown that emodin exhibits anticancer activity in many tumor cell types, there is no available information addressing emodin-affected apoptotic responses in the murine leukemia cell line (WEHI-3) and modulation of the immune response in leukemia mice. We investigated that emodin induced cytotoxic effects in vitro and affected WEHI-3 cells in vivo. This study showed that emodin decreased viability and induced DNA fragmentation in WEHI-3 cells. Cells after exposure to emodin for 24 h have shown chromatin condensation and DNA damage. Emodin stimulated the productions of ROS and Ca2+ and reduced the level of ΔΨm by flow cytometry. Our results from Western blotting suggest that emodin triggered apoptosis of WEHI-3 cells through the endoplasmic reticulum (ER) stress, caspase cascade-dependent and -independent mitochondrial pathways. In in vivo study, emodin enhanced the levels of B cells and monocytes, and it also reduced the weights of liver and spleen compared with leukemia mice. Emodin promoted phagocytic activity by monocytes and macrophages in comparison to the leukemia mice group. In conclusions, emodin induced apoptotic death in murine leukemia WEHI-3 cells and enhanced phagocytosis in the leukemia animal model.