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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 425496, 15 pages
Research Article

Cucurbitacin E Has Neuroprotective Properties and Autophagic Modulating Activities on Dopaminergic Neurons

1Cellular Neurobiology, Department of Medical Biology, Université du Québec à Trois-Rivières, Trois-Rivières, QC, Canada G9A 5H7
2Department of Biochemical Sciences, Faculty of Pharmacy, Charles University in Prague, 500 50 Hradec Kralove, Czech Republic
3Institute of Earth Systems, University of Malta, Msida MSD 2080, Malta
4Department of Psychiatry and Neuroscience, Laval University and CHU Research Center, Québec, QC, Canada G1W 1C2

Received 25 July 2014; Revised 14 November 2014; Accepted 16 November 2014; Published 9 December 2014

Academic Editor: Liang-Jun Yan

Copyright © 2014 Anne-Marie Arel-Dubeau 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.


Natural molecules are under intensive study for their potential as preventive and/or adjuvant therapies for neurodegenerative disorders such as Parkinson’s disease (PD). We evaluated the neuroprotective potential of cucurbitacin E (CuE), a tetracyclic triterpenoid phytosterol extracted from the Ecballium elaterium (Cucurbitaceae), using a known cellular model of PD, NGF-differentiated PC12. In our postmitotic experimental paradigm, neuronal cells were treated with the parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP+) to provoke significant cellular damage and apoptosis or with the potent N,N-diethyldithiocarbamate (DDC) to induce superoxide () production, and CuE was administered prior to and during the neurotoxic treatment. We measured cellular death and reactive oxygen species to evaluate the antioxidant and antiapoptotic properties of CuE. In addition, we analyzed cellular macroautophagy, a bulk degradation process involving the lysosomal pathway. CuE showed neuroprotective effects on MPP+-induced cell death. However, CuE failed to rescue neuronal cells from oxidative stress induced by MPP+ or DDC. Microscopy and western blot data show an intriguing involvement of CuE in maintaining lysosomal distribution and decreasing autophagy flux. Altogether, these data indicate that CuE decreases neuronal death and autophagic flux in a postmitotic cellular model of PD.