Open AccessValproic acid treatment rescues injured tissues after traumatic brain injury
Author(s) -
Ben E. Biesterveld,
Luke Pumiglia,
Ariella Iancu,
Alizeh Shamshad,
Henriette A. Remmer,
Ali Z. Siddiqui,
Rachel O’Connell,
Glenn K. Wakam,
Michael T. Kemp,
Aaron M. Williams,
Manjunath P. Pai,
Hasan B. Alam
Publication year - 2020
Publication title -
the journal of trauma and acute care surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.25
H-Index - 187
eISSN - 2163-0763
pISSN - 2163-0755
DOI - 10.1097/ta.0000000000002918
Subject(s) - traumatic brain injury , valproic acid , neuroprotection , lesion , medicine , pharmacology , glial fibrillary acidic protein , brain damage , histone deacetylase inhibitor , pathology , histone deacetylase , anesthesia , biology , epilepsy , immunohistochemistry , biochemistry , histone , psychiatry , gene
No agents that are specifically neuroprotective are currently approved to emergently treat patients with traumatic brain injury (TBI). The histone deacetylase inhibitor, high-dose valproic acid (VPA) has been shown to have cytoprotective potential in models of combined TBI and hemorrhagic shock, but it has not been tested in an isolated TBI model. We hypothesized that VPA, administered after isolated TBI, will penetrate the injured brain, attenuate the lesion size, and activate prosurvival pathways.