POA.047 - Therapeutic Effects of Vepoloxamer on Neuroprotection and Neurogenesis in Rat After Traumatic Brain Injury
Recommended Citation
Chen L, Xiong Y, Chopp M, Pang H, Zhang Z, Mahmood A, Zhang Y. POA.047 - Therapeutic Effects of Vepoloxamer on Neuroprotection and Neurogenesis in Rat After Traumatic Brain Injury. J Neurotrauma 2025; 42(13-14):e1129.
Document Type
Conference Proceeding
Publication Date
6-12-2025
Publication Title
J Neurotrauma
Keywords
sodium chloride, vepoloxamer, animal cell, animal experiment, animal model, animal tissue, antithrombotic activity, cell loss, cognition, conference abstract, controlled study, diagnosis, female, hippocampus, histopathology, immunofluorescence, immunohistochemistry, inflammation, lesion volume, macrophage, male, microglia, microvascular thrombosis, nervous system development, nervous system inflammation, neuroprotection, nonhuman, rat, therapy effect, traumatic brain injury, Wistar rat
Abstract
Traumatic brain injury (TBI) is a major cause of death and disability worldwide. We have demonstrated that early intervention of Vepoloxamer promotes functional recovery in male and female rats after TBI. The aim of this study is to investigate the potential therapeutic mechanisms of Vepoloxamer on TBI by its antiinflammation and anti-thrombosis effects. Young male Wistar rats, subjected to moderate TBI induced by controlled cortical impact (CCI) injury, were treated randomly with 0 (saline as vehicle) and 300 mg/kg of Vepoloxamer intravenously (IV) 2 h after TBI. Neurological and cognitive functional tests were performed weekly after injury. Animals were killed 3 h, 26 h or 35 days after TBI and brain sections were processed for histopathological and immunohistochemical analyses of lesion volume, neuronal cell loss, neurogenesis, neuroinflammation and microthrombosis. Compared with saline treatment, Vepoloxamer treatment significantly improved neurological and cognitive functional outcomes, reduced lesion volume and prevented hippocampal neuronal cell loss at 26 h and 35 days post-TBI, reduced cerebral microthrombosis formation at 3 h and 26 h post-TBI, reduced the activation of proinflammatory M1 microglia/macrophages and augmented the activation of anti-inflammatory M2 microglia/macrophages in injured cortex at 35 days post-TBI, and enhanced hippocampal neurogenesis at 35 day post-TBI. Collectively, IV Vepoloxamer (300 mg/kg) administrated at 2 h post-TBI provides neuroprotection by anti-inflammation and antimicrothrombosis effects, and enhances neurogenesis in rats post- TBI, indicating that Vepoloxamer may have great potential value for TBI patients.
Volume
42
Issue
13-14
First Page
e1129
