scholarly journals Blast‐induced traumatic brain injury reduces rotarod performance in Sprague‐Dawley male rats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Hibah Omar Awwad ◽  
Larry P Gonzalez ◽  
Megan R. Lerner ◽  
Paul Tompkins ◽  
Daniel J Brackett ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Male Rats ◽  
Sprague Dawley ◽  
Rotarod Performance

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

scholarly journals Enriching neural stem cell and anti‐inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats

2021 ◽  
Author(s):  
Eunyoung Park ◽  
Johnathan G. Lyon ◽  
Melissa Alvarado‐Velez ◽  
Martha I. Betancur ◽  
Nassir Mokarram ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cell ◽  
Electrical Stimulation ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Male Rats ◽  
Anti Inflammatory

Amyloid-β Protein and Neuroglobin Protein as Biomarkers on Brainstem Following Traumatic Brain Injury in Rats

2020 ◽  
Author(s):  
Wenhe Li ◽  
Haijun Zhu ◽  
Yue Liang ◽  
Fang Tong ◽  
Yiwu Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Amyloid Β ◽  
Immunofluorescence Assay ◽  
Amyloid Β Protein ◽  
Sprague Dawley ◽  
Specific Expression ◽  
Western Blot Assay ◽  
Weight Drop

Abstract Background: Biomarkers play an important role in accurate diagnosis of traumatic brain injury (TBI). Due to the complexity and diversity of TBI, it is likely that a single biomarker will not be used for exactly diagnose. Amyloid-beta (Aβ) protein is generated by sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase, which may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain as damage factor of TBI. Its use in diagnosis for TBI is becoming more widespread. Neuroglobin (NGB) protein is great potential to diminish neuronal damage. Most epidemiological evidence suggested that Aβ and NGB may be used as biomarkers on brainstem (BS) following TBI. The aim of this study was to investigate the trend of Aβ and NGB on BS of rats with TBI and to analyze comprehensively them as potential biomarkers. Methods: Adult male Sprague-Dawley rats were subjected to the modified weight-drop model of closed TBI. Biologic behavior observation, histopathological assessments and western blot assay were performed. Aβ and NGB expression indicated temporal changes in BS after TBI. Their accuracy and efficiency of performing these tasks were calculated and statistical comparisons performed.Results: The results of Aβ enable us to speculate that the time points of 3 h, 6 h and 12 h may be crucial points for the diagnosis of TBI. NGB expression in the injured had obvious difference versus the control, the points of 1 h and 3 h were apparently higher than the control, and the groups of 12 h and 48 h were two peaks in the present study. Furthermore, the immunofluorescence assay results supported that Aβ and NGB co-localization in the neuros of BS, and the NGB specific expression in the BS of neurons.Conclusions: Therefore, the expression and change rules of Aβ and NBG in the BS may provide an important foundation for the diagnosis of TBI, damage assessment and therapeutic intervention.

scholarly journals Xenon treatment after severe traumatic brain injury improves locomotor outcome, reduces acute neuronal loss and enhances early beneficial neuroinflammation: a randomized, blinded, controlled animal study

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Rita Campos-Pires ◽  
Haldis Onggradito ◽  
Eszter Ujvari ◽  
Shughoofa Karimi ◽  
Flavia Valeo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
Brain Trauma ◽  
Lesion Volume ◽  
Oxygen Balance ◽  
Sprague Dawley ◽  
Locomotor Deficits

Abstract Background Traumatic brain injury (TBI) is a major cause of morbidity and mortality, but there are no clinically proven treatments that specifically target neuronal loss and secondary injury development following TBI. In this study, we evaluate the effect of xenon treatment on functional outcome, lesion volume, neuronal loss and neuroinflammation after severe TBI in rats. Methods Young adult male Sprague Dawley rats were subjected to controlled cortical impact (CCI) brain trauma or sham surgery followed by treatment with either 50% xenon:25% oxygen balance nitrogen, or control gas 75% nitrogen:25% oxygen. Locomotor function was assessed using Catwalk-XT automated gait analysis at baseline and 24 h after injury. Histological outcomes were assessed following perfusion fixation at 15 min or 24 h after injury or sham procedure. Results Xenon treatment reduced lesion volume, reduced early locomotor deficits, and attenuated neuronal loss in clinically relevant cortical and subcortical areas. Xenon treatment resulted in significant increases in Iba1-positive microglia and GFAP-positive reactive astrocytes that was associated with neuronal preservation. Conclusions Our findings demonstrate that xenon improves functional outcome and reduces neuronal loss after brain trauma in rats. Neuronal preservation was associated with a xenon-induced enhancement of microglial cell numbers and astrocyte activation, consistent with a role for early beneficial neuroinflammation in xenon’s neuroprotective effect. These findings suggest that xenon may be a first-line clinical treatment for brain trauma.

Outcome measures from experimental traumatic brain injury in male rats vary with the complete temporal biomechanical profile of the injury event

2020 ◽  
Vol 98 (10) ◽  
pp. 2027-2044
Author(s):  
Radia Abdul‐Wahab ◽  
Mathew T. Long ◽  
Rafael Ordaz ◽  
Bruce G. Lyeth ◽  
Bryan J. Pfister
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Outcome Measures ◽  
Male Rats ◽  
Injury Event ◽  
Experimental Traumatic Brain Injury

scholarly journals Administration of a 20-Hydroxyeicosatetraenoic Acid Synthesis Inhibitor Improves Outcome in a Rat Model of Pediatric Traumatic Brain Injury

2019 ◽  
Vol 41 (3-4) ◽  
pp. 166-176 ◽  
Author(s):  
Shiyu Shu ◽  
Zhi Zhang ◽  
Dawn Spicer ◽  
Ewa Kulikowicz ◽  
Ke Hu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ischemia Reperfusion ◽  
Memory Task ◽  
Male Rats ◽  
Lesion Volume ◽  
Hydroxyeicosatetraenoic Acid ◽  
Post Injury ◽  
Synthesis Inhibitor ◽  
Tnf Α

The arachidonic acid pathway metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to ischemia/reperfusion brain injury. Inhibition of 20-HETE formation can protect the developing brain from global ischemia. Here, we examined whether treatment with the 20-HETE synthesis inhibitor N-hydroxy-N-4-butyl-2-methylphenylformamidine (HET0016) can protect the immature brain from traumatic brain injury (TBI). Male rats at postnatal day 9–10 underwent controlled cortical impact followed by intraperitoneal injection with vehicle or HET0016 (1 mg/kg, 5 min and 3 h post-injury). HET0016 decreased the lesion volume by over 50% at 3 days of recovery, and this effect persisted at 30 days as the brain matured. HET0016 decreased peri-lesion gene expression of proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-1β [IL-1β]) at 1 day and increased reparative cytokine (IL-4, IL-10) expression at 3 days. It also partially preserved microglial ramified processes, consistent with less activation. HET0016 decreased contralateral hindlimb foot faults and improved outcome on the novel object recognition memory task 30 days after TBI. In cultured BV2 microglia, HET0016 attenuated the lipopolysaccharide-evoked increase in release of TNF-α. Our data show that HET0016 improves acute and long-term histologic and functional outcomes, in association with an attenuated neuroinflammatory response after contusion of an immature rat brain.

scholarly journals Repeated Mild Traumatic Brain Injury Results in Long-Term White-Matter Disruption

2014 ◽  
Vol 34 (4) ◽  
pp. 715-723 ◽  
Author(s):  
Virginia Donovan ◽  
Claudia Kim ◽  
Ariana K Anugerah ◽  
Jacqueline S Coats ◽  
Udochuwku Oyoyo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Mild Traumatic Brain Injury ◽  
Diffusion Tensor ◽  
Ex Vivo ◽  
Health Concern ◽  
Sprague Dawley ◽  
G Ratio

Mild traumatic brain injury (mTBI) is an increasing public health concern as repetitive injuries can exacerbate existing neuropathology and result in increased neurologic deficits. In contrast to other models of repeated mTBI (rmTBI), our study focused on long-term white-matter abnormalities after bilateral mTBIs induced 7 days apart. A controlled cortical impact (CCI) was used to induce an initial mTBI to the right cortex of Single and rmTBI Sprague Dawley rats, followed by a second injury to the left cortex of rmTBI animals. Shams received only a craniectomy. Ex vivo diffusion tensor imaging (DTI), transmission electron microscopy (TEM), and histology were performed on the anterior corpus callosum at 60 days after injury. The rmTBI animals showed a significant bilateral increase in radial diffusivity (myelin), while only modest changes in axial diffusivity (axonal) were seen between the groups. Further, the rmTBI group showed an increased g-ratio and axon caliber in addition to myelin sheath abnormalities using TEM. Our DTI results indicate ongoing myelin changes, while the TEM data show continuing axonal changes at 60 days after rmTBI. These data suggest that bilateral rmTBI induced 7 days apart leads to progressive alterations in white matter that are not observed after a single mTBI.

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