The NADPH oxidase NOX2 mediates loss of parvalbumin interneurons in traumatic brain injury: human autoptic immunohistochemical evidence.

ABSTRACT: Pharmacological interventions for traumatic brain injury (TBI) are limited. Together with parvalbumin (PV) loss, increased production of reactive oxygen species (ROS) by the NADPH oxidase NOX enzymes represents a key step in TBI. Here, we investigated the contribution of NOX2-derived oxidative stress to the loss of PV immunoreactivity associated to TBI, performing immunohistochemistry for NOX2, 8-hydroxy-2'-deoxyguanosine (8OHdG) and PV on post mortem brain samples of subjects died following TBI, subjects died from spontaneous intracerebral hemorrhage (SICH) and controls (CTRL). We detected an increased NOX2 expression and 8OHdG immunoreactivity in subjects died from TBI with respect to CTRL and SICH. NOX2 increase was mainly observed in GABAergic PV-positive interneurons, with a minor pre

SUBMITTER: Schiavone S 

PROVIDER: S-EPMC5562735 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature