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BioMed Research International
Volume 2014 (2014), Article ID 980657, 8 pages
Research Article

Low Dose of Valproate Improves Motor Function after Traumatic Brain Injury

1Department of Anesthesiology, Taipei Medical University-Wan Fang Hospital, Taipei Medical University, Taipei 116, Taiwan
2Department of Neurosurgery, China Medical University Hospital, China Medical University, Taipei Branch, Taipei, Taiwan
3Department of Otolaryngology, Clinical Research Center, School of Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
4Department of Neurosurgery, Clinical Research Center, Graduate Institute of Injury Prevention and Control, Wan Fang Hospital, Taipei Medical University, No. 111, Section 3, Hsing-Long Road, Taipei 116, Taiwan
5Graduate Institute of Biomedical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan

Received 30 November 2013; Accepted 14 December 2013; Published 6 February 2014

Academic Editor: Wei Chiao Chang

Copyright © 2014 Yu-Ting Tai 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. Traumatic brain injuries (TBIs) are a major health care problem worldwide. Approximately 1.5 million new TBI cases occur annually in the United States, with mortality rates ranging between 35% and 40% in severe patients. Despite the incidence of these injuries and their substantial socioeconomic implications, no specific pharmacological intervention is available for clinical use. Several studies have indicated that 300 mg/kg or 400 mg/kg of valproate (VPA) exhibits neuroprotective effects in animal models. However, humans cannot tolerate high doses of VPA. This study aims to investigate whether 30 mg/kg of VPA administered to rats affects TBIs. Methods. We used a rat model to test the effects of 30 mg/kg of VPA on TBIs. Molecular identifications for histone acetylation and phosphorylation of cAMP response element-binding protein (CREB) and phosphorylated extracellular signal regulated kinase (ERK) were performed. Results. The results indicated that treating adult rats with VPA after TBIs significantly decreased the contusion volume and recovery of contusion-related skilled forelimb reaching deficits. Applying VPA also increased histone acetylation, p-ERK, and p-CREB expression in the brain. Furthermore, applying VPA reduced inflammation, glial fibrillary acidic protein activation, and apoptosis. Conclusion. This study found that 30 mg/kg of VPA assists in treating TBIs in rat models.