scholarly journals Activation of NF-κB Mediates Astrocyte Swelling and Brain Edema in Traumatic Brain Injury

2014 ◽  
Vol 31 (14) ◽  
pp. 1249-1257 ◽  
Author(s):  
Arumugam R. Jayakumar ◽  
Xiao Y. Tong ◽  
Roberto Ruiz-Cordero ◽  
Amade Bregy ◽  
John R. Bethea ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Astrocyte Swelling

Mechanism of Aquaporin-4 Up-Regulation After Traumatic Brain Injury and Preventative Action of Astragalus Polysaccharides in Mice

2021 ◽  
Vol 11 (6) ◽  
pp. 1037-1045
Author(s):  
Bin Li ◽  
Honggang Yuan ◽  
Huibing Li ◽  
Baochang Luo ◽  
Xiaoping Yu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Chemical Compound ◽  
Neurological Deficits ◽  
Signal Molecules ◽  
Astragalus Polysaccharides ◽  
Astrocyte Swelling ◽  
Pre Treatment

Here, we aimed to clarify the anti-inflammatory function of Astragalus Polysaccharides (APS), a chemical compound derived from Astragalus membranaceus, and the action of AQP4 on brain injury. We hypothesized that APS could improve the traumatic brain injury (TBI) outcome via inhibiting expression of AQP4 in astrocytes. The present study elucidated that AQP4 was up-regulated and was effectively blocked by APS in mice with severe controlled cortical impact (CCI). Pre-treatment with APS effectively inhibited the up-regulation of AQP4 and diminished the neurological deficits in mice. Additionally, primary astrocytes treated with mechanically-injured astrocyte supernatant, to mimic TBI in vitro, showed a significant up-regulation in swelling. We confirmed various signal molecules (NF-ĸB, MAPKs, and ERK) to have a role in astrocyte swelling, after activation in trauma, and to be involved in the up-regulation of AQP4. These signal molecules also significantly decreased with APS treatment. In conclusion, our study suggests that APS attenuated neurological deficits and brain edema by decreasing AQP4 up-regulation in astrocytes following TBI in mice, via reducing NF-ĸB, MAPKs, and the ERK signal molecules.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury

2014 ◽  
Vol 28 (6) ◽  
pp. 739-745 ◽  
Author(s):  
Weichuan Wu ◽  
Runfa Tian ◽  
Shuyu Hao ◽  
Feifan Xu ◽  
Xiang Mao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Ethanol Intake ◽  
High Ethanol

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

2014 ◽  
Vol 76 ◽  
pp. S22
Author(s):  
Kenji Dohi ◽  
Andrej Kovac ◽  
Michelle Erickson ◽  
Brian C Kraemer ◽  
Takeki Ogawa ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Drinking Water ◽  
Brain Injury ◽  
Brain Edema

NKCC1-mediated traumatic brain injury-induced brain edema and neuron death via Raf/MEK/MAPK cascade

2008 ◽  
Vol 36 (3) ◽  
pp. 917-922 ◽  
Author(s):  
Kwok-Tung Lu ◽  
Nai-Chi Cheng ◽  
Chang-Yen Wu ◽  
Yi-Ling Yang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Mapk Cascade ◽  
Neuron Death

scholarly journals Blockade of endothelin ETB receptor ameliorates brain edema by regulation of astrocyte-derived factors after traumatic brain injury in mice

2019 ◽  
Vol 92 (0) ◽  
pp. 2-YIA-20
Author(s):  
Shotaro Michinaga ◽  
Ryusei Nakaya ◽  
Chihiro Fukutome ◽  
Yukiko Minato ◽  
Anna Inoue ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema

scholarly journals Steroids for delayed cerebral edema after traumatic brain injury

2021 ◽  
Vol 12 ◽  
pp. 46
Author(s):  
G. Lakshmi Prasad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Head Injuries ◽  
Experimental Studies ◽  
Symptomatic Improvement ◽  
High Dose ◽  
The Mean ◽  
Key Aspects

Background: Brain edema is a common phenomenon after traumatic brain injury (TBI) resulting in increased intracranial pressure and subsequent neurological deterioration. Experimental studies have proven that brain edema is biphasic (cytotoxic followed by vasogenic). Till date, all studies, including the corticosteroid randomization after significant head injury (HI) trial, have used high-dose steroids in the acute period during which the edema is essentially cytotoxic in nature. No clinical data exist pertaining to delayed cerebral edema (vasogenic) and steroids. Methods: Patients who had received steroids for delayed cerebral edema after TBI were retrospectively analyzed over a 2-year period. Steroid dose, timing of steroid prescription, time to improvement of symptoms, and complications were noted. Results: There were six males and three females. Mean age was 41.1 years. There were no severe HI cases. All subjects had cerebral contusions on imaging. Dexamethasone was the preferred steroid starting with 12 mg/day and tapered in 5–7 days. The mean interval to steroid administration after trauma was 7 days. The mean duration of steroid prescription was 6.3 days. All patients had complete symptomatic improvement. The mean time to symptom resolution was 3.8 days. No patients experienced any complications pertinent to steroid usage. Conclusion: This is the first study to document efficacy of steroids for delayed cerebral edema after TBI, at least in mild/moderate head injuries. The timing of steroid usage and dose of steroids is key aspects that might determine its efficacy in TBI which was the drawbacks of the previous studies. Future prospective trials with the above factors in consideration may confirm/refute above findings.

The Synergistic Effect of Acute Subdural Hematoma Combined with Diffuse Traumatic Brain Injury on Brain Edema

2000 ◽  
pp. 213-216
Author(s):  
Y. Tomita ◽  
S. Sawauchi ◽  
A. Beaumont ◽  
Anthony Marmarou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Synergistic Effect ◽  
Brain Edema ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma

Arginine Vasopressin V1a Receptor-Deficient Mice Have Reduced Brain Edema and Secondary Brain Damage following Traumatic Brain Injury

2013 ◽  
Vol 30 (16) ◽  
pp. 1442-1448 ◽  
Author(s):  
Katrin Rauen ◽  
Raimund Trabold ◽  
Christian Brem ◽  
Nicole A. Terpolilli ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Brain Damage ◽  
Arginine Vasopressin ◽  
Secondary Brain Damage ◽  
V1a Receptor ◽  
Vasopressin V1a Receptor ◽  
Deficient Mice

scholarly journals HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

2018 ◽  
Vol 46 (6) ◽  
pp. 2532-2542 ◽  
Author(s):  
Lijun Yang ◽  
Feng Wang ◽  
Liang Yang ◽  
Yunchao Yuan ◽  
Yan Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Therapeutic Potential ◽  
High Mobility ◽  
Neurological Injury ◽  
Secondary Brain Injury ◽  
Cell Degeneration ◽  
Injured Brain ◽  
Walking Tests

Background/Aims: Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. Methods: TBI was induced by controlled cortical impact (CCI) in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan’s blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. Results: HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Conclusion: Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI.

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