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