Low dose of valproate improves motor function after traumatic brain injury

Yu Ting Tai, Wen Yuan Lee, Fei Peng Lee, Tien Jen Lin, Chia Lin Shih, Jia Yi Wang, Wen Ta Chiu, Kuo Sheng Hung

研究成果: 雜誌貢獻文章

16 引文 (Scopus)

摘要

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.
原文英語
文章編號980657
期刊BioMed Research International
2014
DOIs
出版狀態已發佈 - 2014

指紋

Valproic Acid
Brain
Rats
Acetylation
Cyclic AMP Response Element-Binding Protein
Contusions
Extracellular Signal-Regulated MAP Kinases
Histones
Phosphorylation
Forelimb
Traumatic Brain Injury
Glial Fibrillary Acidic Protein
Neuroprotective Agents
Health care
Animals
Animal Models
Chemical activation
Pharmacology
Apoptosis
Inflammation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

引用此文

Low dose of valproate improves motor function after traumatic brain injury. / Tai, Yu Ting; Lee, Wen Yuan; Lee, Fei Peng; Lin, Tien Jen; Shih, Chia Lin; Wang, Jia Yi; Chiu, Wen Ta; Hung, Kuo Sheng.

於: BioMed Research International, 卷 2014, 980657, 2014.

研究成果: 雜誌貢獻文章

@article{b524b0f6bf764b06a9c89bf2262dc47c,
title = "Low dose of valproate improves motor function after traumatic brain injury",
abstract = "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.",
author = "Tai, {Yu Ting} and Lee, {Wen Yuan} and Lee, {Fei Peng} and Lin, {Tien Jen} and Shih, {Chia Lin} and Wang, {Jia Yi} and Chiu, {Wen Ta} and Hung, {Kuo Sheng}",
year = "2014",
doi = "10.1155/2014/980657",
language = "English",
volume = "2014",
journal = "BioMed Research International",
issn = "2314-6133",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Low dose of valproate improves motor function after traumatic brain injury

AU - Tai, Yu Ting

AU - Lee, Wen Yuan

AU - Lee, Fei Peng

AU - Lin, Tien Jen

AU - Shih, Chia Lin

AU - Wang, Jia Yi

AU - Chiu, Wen Ta

AU - Hung, Kuo Sheng

PY - 2014

Y1 - 2014

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84896885768&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84896885768&partnerID=8YFLogxK

U2 - 10.1155/2014/980657

DO - 10.1155/2014/980657

M3 - Article

C2 - 24689067

AN - SCOPUS:84896885768

VL - 2014

JO - BioMed Research International

JF - BioMed Research International

SN - 2314-6133

M1 - 980657

ER -