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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 354840, 9 pages
Research Article

Evodiamine Induces Transient Receptor Potential Vanilloid-1-Mediated Protective Autophagy in U87-MG Astrocytes

1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
2Department of Neurosurgery, Taipei City Hospital Ren-Ai Branch, Taipei, Taiwan
3Department of Biochemistry, School of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
4Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan
5Department of Neurosurgery, Taipei Municipal Wan-Fang Hospital, Taipei, Taiwan
6Department of Surgery, College of Medicine, Taipei Medical University, Taiwan
7Division of Cardiac Surgery, Cathy General Hospital, Taipei, Taiwan
8Traditional Herbal Medicine Research Center, Taipei Medical University Hospital, Taipei, Taiwan

Received 21 October 2013; Accepted 23 November 2013

Academic Editor: Joen-Rong Sheu

Copyright © 2013 Ann-Jeng Liu 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.


Cerebral ischemia is a leading cause of mortality and morbidity worldwide, which results in cognitive and motor dysfunction, neurodegenerative diseases, and death. Evodiamine (Evo) is extracted from Evodia rutaecarpa Bentham, a plant widely used in Chinese herbal medicine, which possesses variable biological abilities, such as anticancer, anti-inflammation, antiobesity, anti-Alzheimer’s disease, antimetastatic, antianoxic, and antinociceptive functions. But the effect of Evo on ischemic stroke is unclear. Increasing data suggest that activation of autophagy, an adaptive response to environmental stresses, could protect neurons from ischemia-induced cell death. In this study, we found that Evo induced autophagy in U87-MG astrocytes. A scavenger of extracellular calcium and an antagonist of transient receptor potential vanilloid-1 (TRPV-1) decreased the percentage of autophagy accompanied by an increase in apoptosis, suggesting that Evo may induce calcium-mediated protective autophagy resulting from an influx of extracellular calcium. The same phenomena were also confirmed by a small interfering RNA technique to knock down the expression of TRPV1. Finally, Evo-induced c-Jun N-terminal kinases (JNK) activation was reduced by a TRPV1 antagonist, indicating that Evo-induced autophagy may occur through a calcium/c-Jun N-terminal kinase (JNK) pathway. Collectively, Evo induced an influx of extracellular calcium, which led to JNK-mediated protective autophagy, and this provides a new option for ischemic stroke treatment.