scholarly journals Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jinn-Rung Kuo ◽  
Chong-Jeh Lo ◽  
Ching-Ping Chang ◽  
Mao- Tsun Lin ◽  
Chung-Ching Chio
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Jugular Vein ◽  
External Jugular Vein ◽  
Motor Deficits ◽  
Sham Operation ◽  
Brain Cooling ◽  
Cerebral Contusion ◽  
Oxide Synthase

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.

scholarly journals Selective Brain Cooling Reduces Motor Deficits Induced by Combined Traumatic Brain Injury, Hypoxemia and Hemorrhagic Shock

2018 ◽  
Vol 9 ◽  
Author(s):  
Lai Yee Leung ◽  
Katherine Cardiff ◽  
Xiaofang Yang ◽  
Bernard Srambical Wilfred ◽  
Janice Gilsdorf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Hemorrhagic Shock ◽  
Motor Deficits ◽  
Brain Cooling ◽  
Selective Brain Cooling

scholarly journals Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-αContents and by Stimulating Newly Formed Neurogenesis

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chong-Un Cheong ◽  
Ching-Ping Chang ◽  
Chien-Ming Chao ◽  
Bor-Chih Cheng ◽  
Chung-Zhing Yang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Quantitative Determination ◽  
Enzyme Immunoassay ◽  
Immunofluorescence Staining ◽  
Motor Deficits ◽  
Etanercept Therapy ◽  
Cerebral Contusion ◽  
Brain Tissues

It remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF-αand/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury is assessed in all rats the day prior to and 7 days after surgery. The numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain injury that occurred during TBI were counted by immunofluorescence staining. Enzyme immunoassay for quantitative determination of TNF-αor etanercept in brain tissues is also performed. Seven days after systemic administration of etanercept, levels of etanercept can be detected in the contused brain tissues. In addition, neurological and motor deficits, cerebral contusion, and increased brain TNF-αcontents caused by TBI can be attenuated by etanercept therapy. Furthermore, the increased numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain tissues caused by TBI can be potentiated by etanercept therapy. These findings indicate that systemically administered etanercept may penetrate directly into the contused brain tissues and may improve outcomes of TBI by reducing brain contents of TNF-αand by stimulating newly formed neurogenesis.

scholarly journals Disrupting nNOS–PSD95 Interaction Improves Neurological and Cognitive Recoveries after Traumatic Brain Injury

2020 ◽  
Vol 30 (7) ◽  
pp. 3859-3871 ◽  
Author(s):  
Wenrui Qu ◽  
Nai-Kui Liu ◽  
Xiangbing Wu ◽  
Ying Wang ◽  
Yongzhi Xia ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
P38 Mapk ◽  
Brain Lesion ◽  
Mapk Signaling ◽  
Motor Deficits ◽  
Neuronal Cultures ◽  
Normal Brain ◽  
Lesion Volume ◽  
Oxide Synthase

Abstract Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI). However, directly inhibiting NMDARs or nNOS produces adverse side effects because they play key physiological roles in the normal brain. Since interaction of nNOS–PSD95 is a key step in NMDAR-mediated excitotoxicity, we investigated whether disrupting nNOS–PSD95 interaction with ZL006, an inhibitor of nNOS–PSD95 interaction, attenuates NMDAR-mediated excitotoxicity. In cortical neuronal cultures, ZL006 treatment significantly reduced glutamate-induced neuronal death. In a mouse model of controlled cortical impact (CCI), administration of ZL006 (10 mg/kg, i.p.) at 30 min postinjury significantly inhibited nNOS–PSD95 interaction, reduced TUNEL- and phospho-p38-positive neurons in the motor cortex. ZL006 treatment also significantly reduced CCI-induced cortical expression of apoptotic markers active caspase-3, PARP-1, ratio of Bcl-2/Bax, and phosphorylated p38 MAPK (p-p38). Functionally, ZL006 treatment significantly improved neuroscores and sensorimotor performance, reduced somatosensory and motor deficits, reversed CCI-induced memory deficits, and attenuated cognitive impairment. Histologically, ZL006 treatment significantly reduced the brain lesion volume. These findings collectively suggest that blocking nNOS–PSD95 interaction represents an attractive strategy for ameliorating consequences of TBI and that its action is mediated via inhibiting neuronal apoptosis and p38 MAPK signaling.

Induction of nitric oxide synthase by traumatic brain injury

2001 ◽  
Vol 123 (2-3) ◽  
pp. 142-149 ◽  
Author(s):  
Yoshiyuki Orihara ◽  
Kazuya Ikematsu ◽  
Ryouichi Tsuda ◽  
Ichiro Nakasono
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase

Reduction of the Neurological Deficit in Mice with Traumatic Brain Injury by Nitric Oxide Synthase Inhibitors

1996 ◽  
Vol 13 (4) ◽  
pp. 209-214 ◽  
Author(s):  
CHRISTIAN MÉSENGE ◽  
CATHERINE VERRECCHIA ◽  
MONIQUE ALLIX ◽  
ROGER R. BOULU ◽  
MICHEL PLOTKINE
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nitric Oxide Synthase ◽  
Neurological Deficit ◽  
Nitric Oxide Synthase Inhibitors ◽  
Oxide Synthase

N-methyl-D-aspartate preconditioning improves short-term motor deficits outcome after mild traumatic brain injury in mice

2009 ◽  
pp. n/a-n/a ◽  
Author(s):  
Tayana Costa ◽  
Leandra C. Constantino ◽  
Bruna P. Mendonça ◽  
Josimar G. Pereira ◽  
Bruno Herculano ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Motor Deficits ◽  
Short Term
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