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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4202437, 11 pages
Research Article

SOD2 Mediates Amifostine-Induced Protection against Glutamate in PC12 Cells

1Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
2Department of Anesthesiology, Xi’an No. 4 Hospital, Xi’an 710032, China
3Department of General Surgery, Fuzhou General Hospital of Nanjing Military Command, Fuzhou 350025, China
4Department of Anesthesiology, Wuhan General Hospital of Guangzhou Military Command, Wuhan 430070, China
5Department of Gastrointestinal Surgery, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi’an 710032, China

Received 15 July 2015; Revised 31 August 2015; Accepted 1 September 2015

Academic Editor: Ryuichi Morishita

Copyright © 2016 Ji Jia 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.


Background. Cytoprotectant amifostine attenuates radiation-induced oxidative injury by increasing intracellular manganese superoxide dismutase (SOD2) in peripheral tissue. However, whether amifostine could protect neuronal cells against oxidative injury has not been reported. The purpose of this study is to explore the protection of amifostine in PC12 cells. Methods. PC12 cells exposed to glutamate were used to mimic neuronal oxidative injury. SOD assay kit was taken to evaluate intracellular Cu/Zn SOD (SOD1) and SOD2 activities; western blot analysis and immunofluorescence staining were performed to investigate SOD2 protein expression; MTT, lactate dehydrogenase (LDH), release and cell morphology were used to evaluate cell injury degree, and apoptotic rate and cleaved caspase-3 expression were taken to assess apoptosis; mitochondrial superoxide production, intracellular reactive oxygen species (ROS), and glutathione (GSH) and catalase (CAT) levels were evaluated by reagent kits. Results. Amifostine increased SOD2 activity and expression, decreased cell injury and apoptosis, reduced mitochondrial superoxide production and intracellular ROS generation, and restored intracellular GSH and CAT levels in PC12 cells exposed to glutamate. SOD2-siRNA, however, significantly reversed the amifostine-induced cytoprotective and antioxidative actions. Conclusion. SOD2 mediates amifostine-induced protection in PC12 cells exposed to glutamate.