Article

Hydrogen in Drinking Water Reduces Brain Edema after Traumatic Brain Injury in Mice

November 2014
Free Radical Biology and Medicine 76:S22

DOI:10.1016/j.freeradbiomed.2014.10.471

Authors:

Kenji Dohi

Showa University

Andrej Kovac

Slovak Academy of Sciences

Michelle Erickson

VA Medical Center, Seattle

Brian C Kraemer

University of Washington Seattle

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ResearchGate has not been able to resolve any references for this publication.

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Traumatic brain injury (TBI) is a major cause of death and disability in children and young adults worldwide. Therefore, we investigated the role of AG490 in regulating brain oedema, expression of CD40 and neurological function after TBI. Sprague Dawley rats (n = 240) were randomly divided into a sham operation group, TBI+saline group and TBI+AG490 (JAK/STAT inhibitor) group. Members of each ... [Show full abstract] group were euthanized at 6, 12, 24 or 72 hours after injury. Neurological severity score (NSS) was used to evaluate the severity of neurological damage. Brain water was quantitated by wet/dry weight method. The expression of CD40 was assessed by flow cytometry. In both the TBI+saline group and the TBI+AG490 group, the brain water content was elevated after TBI, reached a peak at 24-hour and remained high for the rest of the period investigated; the expression of CD40 reached a peak 24 hours after TBI; the NSS was elevated after TBI and then decreased after 6 hours. Elevations in the level of CD40, degree of brain edema and NSS after TBI were significantly reduced in TBI+AG490 group. Inhibition of the JAK/STAT signalling pathway reduces brain oedema, decreases the expression of CD40 and exerts neuroprotective effects after TBI.

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Purpose Cerebral edema is usually assessed with mean ADC value obtained with MRI. We aimed to use parametric response mapping (PRM), a voxel-based analysis, in a rat model of traumatic brain injury (TBI) to characterize the cerebral edema and to compare findings to those obtained with the classical global mean ADC analysis. Ultimately we wished to test whether early PRM analysis could identify ... [Show full abstract] the vasogenic or cellular edematous pattern two hours after trauma. Materials and Methods Experiments were conducted in a rat model of TBI in accordance with French Government guidelines. Eighteen traumatic brain-injured rats (TBI group) were compared to 7 sham-operated rats (Sham group). Diffusion-weighted images were acquired before and immediately (H0), 60min (H1) and 120min (H2) after the trauma. Two regions of interest (ROI) including cortex (cortical-ROI) and the whole brain (brainROI) were manually delineated. Results Averaged ADC value in cortical-ROI was significantly reduced at H2 in the TBI group versus Sham group (715±24 vs 781±16 µm²/sec; p=0.04), not in brain-ROI (748±27 vs 801±18 µm²/sec; p=0.32). By contrast, PRM values were significantly changed in these two ROIs at as soon as H1 in the TBI group (27.5±4% of the voxels beyond the PRM threshold in TBI group vs 5.1±1% in sham group; p<0.01). PRM was able to identify the nature of post traumatic cerebral edema: vasogenic, cellular or mixed pattern. ADC data obtained immediately after TBI and analyzed using PRM correlated with ADC data obtained at H2. Conclusion The PRM approach is more sensitive than averaged ADC at detecting and identifying post-traumatic brain edema. It is able to PRM might be a promising tool to individualize the management of patients with posttraumatic brain edema.

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Statement of significance: Traumatic brain injury (TBI) is a life-threatening condition characterized by severe brain swelling and is currently treated by a two-stage surgical procedure. Complications associated with the two-stage surgical intervention include the occurrence of the condition termed syndrome of the trephined; however, the condition is completely reversible once the secondary ... [Show full abstract] surgery is performed. A desirable TBI treatment would include a single surgical intervention to avoid syndrome of the trephined altogether. The first hurdle in reaching the overall goal is to develop a pliable hydrogel material which can regenerate the patient's bone. The development of a pliable hydrogel technology would greatly impact the field of bone regeneration for TBI application and other areas of bone regeneration.

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A common pathology in Traumatic brain injury (TBI) is brain edema that develops within hours of impact. It causes increased intracranial pressure (ICP), and nerve damage. It was shown that Walnut kernel (WK) has a large amount of phenolic compounds with beneficial effects on human health due to antioxidant and anti-inflammatory properties. The present study was designed to investigate the effect ... [Show full abstract] of WK feeding on brain edema, neurological score and neuronal degeneration in male rat after traumatic brain injury. The diffuse TBI was induced in adult male rats using Marmarou's method. Sixty days prior to the injury, WK was added to ordinary food (6% percent of daily food). Experimental groups are included sham (no TBI and no WK), control (TBI and no WK) and treatment (TBI and WK). Brain edema and neuronal injury were measured 72 h after TBI. Veterinary Coma Scale (VCS) and ICP were assessed at -1, 4, 24, 48 and 72 h after TBI. Brain water content and ICP in treatment group decreased as compared to the control. Besides, VCS at 24, 48 and 72 h after TBI showed a significant increase in treatment group in comparison with control. Based on our data, WK pre-treatment may reduce pathological parameters after TBI in male rats.

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Investigation of Morphological Change of Lateral and Midline Fluid Percussion Injury in Rats, Using...

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OBJECTIVE: Investigating the time course of morphological changes in experimental traumatic brain injury (TBI) in vivo helps to clarify the mechanism of TBI and develop new therapeutic modalities. We examined the morphological changes in experimental TBI, using magnetic resonance imaging (MRI) in a rat model. METHODS: We produced lateral fluid percussion injury (LFP) and midline fluid percussion ... [Show full abstract] injury (MFP) in rats, using the Yamaki fluid percussion device. The rats were divided into four groups: LFP, MFP, sham LFP, and sham MFP. MRI was performed with a 4.7-T magnetic resonance apparatus 2 days and 90 days after the induction of injury. T1-, T2-, and T2*-weighted images were obtained using a surface coil. RESULTS: Hemorrhage, contusion, and brain edema in LFP models were detected on the 2nd day after injury, and the necrotic tissue was absorbed and replaced by cerebrospinal fluid on the 90th day. In MFP animals, we detected a small hemorrhage in the corpus callosum with minimal brain edema around the hemorrhage on the 2nd day after injury, and on the 90th day, enlarged ventricles and cisterns were observed, indicating brain atrophy. CONCLUSION: MRI, therefore, is useful for plotting morphological changes in experimental TBI in vivo. We report the novel and clinically important finding of brain atrophy after experimental TBI.

Last Updated: 05 Jul 2022

Hydrogen in Drinking Water Reduces Brain Edema after Traumatic Brain Injury in Mice

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