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Updated: May 2, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
NADPH oxidase inhibition improves neurological outcome in experimental traumatic brain injury
Xin-Yu Lu1, Han-Dong Wang2, Jian-Guo Xu2
1Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, China; Department of Neurosurgery, People's Hospital Affiliated to Jiangsu University, Zhenjiang, Jiangsu Province, China.
Purpose:
Traumatic brain injury (TBI) is a worldwide health problem with oxidative stress recognized as a major pathogenetic factor. The present experimental study was designed to explore the neuroprotective effect of NADPH oxidase (NOX) inhibitor, apocynin, on mouse TBI.
Methods:
Moderately severe weight-drop impact head injury was induced in adult male mice, randomly divided into four groups: sham, TBI, TBI+vehicle and TBI+apocynin treatment. Apocynin (50 mg/kg) was injected intraperitoneally 30 min before TBI. The expression of NOX2 protein was investigated using immunoblotting techniques 1 and 24h after TBI. Neurological score was evaluated 24h after TBI. Blood-brain barrier disruption was detected by Evans blue extravasation and cortical apoptosis was analyzed by TUNEL assay. Additionally, we assessed tissue levels of malondialdehyde (MDA).
Results:
NOX2 expression increased rapidly following TBI in male mice, with an early peak at 1h, followed by a second peak at 24h. Pre-treatment with the NOX inhibitor, apocynin markedly inhibited NOX2 expression. Apocynin also attenuated MDA levels and TBI-induced blood-brain barrier dysfunction. In addition apocynin significantly attenuated TBI-induced neurological deficits and cortical apoptosis.
Conclusion:
Pre-treatment with apocynin effectively attenuates markers of cerebral oxidative stress after TBI, thus supporting the hypothesis that apocynin is a potential neuroprotectant and adjunct therapy for TBI patients.
