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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 4517486, 13 pages
Research Article

Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells

1Center for Bioresources & Drug Discovery and School of Biosciences & Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, China
2School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071, China
3Hunan Auragene Biotech Co., Ltd., Changsha 410013, China
4Guangdong Province Key Laboratory for Biotechnology Drug Candidates, Guangdong Pharmaceutical University, Guangzhou 510006, China

Correspondence should be addressed to Zebo Huang; nc.ude.updg@gnauhobez

Received 28 January 2017; Revised 17 April 2017; Accepted 2 May 2017; Published 11 June 2017

Academic Editor: Giuseppe Filomeni

Copyright © 2017 Haifeng Li 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.

Supplementary Material

FIGURE 1S: Effect of tanshinone IIA on cell viability and proliferation in SH-SY5Y cells under glutamate intoxication. (a) Trypan Blue exclusion rate of the SH-SY5Y cells pretreated with tanshinone IIA at the indicated concentrations for 24 h and then exposed to 10 mM glutamate for another 24 h. (b) BrdU incorporation rate of the SH-SY5Y cells treated as in (a). All data are normalized to the cells without tanshinone IIA treatment and glutamate exposure and presented as mean ± SEM of three independent experiments. Tan IIA, tanshinone IIA. Glu, glutamate. * p < 0.05, compared to the cells exposed to glutamate alone.

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