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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 728751, 10 pages
Research Article

Curcumin Inhibits Mitochondrial Injury and Apoptosis from the Early Stage in EAE Mice

1Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
2Department of Neurology, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, China
3Department of Medicine, Drexel University College of Medicine, Philadelphia, PA 19129, USA

Received 18 January 2014; Accepted 27 March 2014; Published 27 April 2014

Academic Editor: Luisa Minghetti

Copyright © 2014 Jinzhou Feng 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.


The exact pathophysiological change concerning mitochondrial injury and oligodendrocyte apoptosis in MS and EAE model is still unknown. Whether curcumin is able to inhibit mitochondrial injury and suppress the apoptosis in the early stages of MS/EAE is still unclear. We first explored mitochondrial injury and apoptosis at different time points p.i. in C57 BL/6 EAE mice. We then explored the effects of curcumin on mitochondria and apoptosis. Results showed that mitochondrial injury can be observed 3 days p.i. Apoptosis in the spinal cord occurred 3 days p.i. and the apoptotic cells were shown to be oligodendrocytes and neuronal cells. Curcumin significantly reduced the number of apoptotic cells and inhibited the upregulation of cyt-c, caspase-9, and caspase-3 at 7 days p.i. in the EAE mice. These observations demonstrate that mitochondrial injury and oligodendrocyte/neuronal apoptosis occur in the early stages of EAE. Curcumin can inhibit apoptosis in EAE mice which maybe act through protection of mitochondrial injury and inhibition of the intrinsic apoptotic pathway.