An Effective NADPH Oxidase 2 Inhibitor Provides Neuroprotection and Improves Functional Outcomes in Animal Model of Traumatic Brain Injury

2020 ◽  
Vol 45 (5) ◽  
pp. 1097-1106
Author(s):  
Mengwei Wang ◽  
Le Luo
Keyword(s):  
Traumatic Brain Injury ◽  
Animal Model ◽  
Brain Injury ◽  
Nadph Oxidase ◽  
Functional Outcomes ◽  
Nadph Oxidase 2

scholarly journals NADPH Oxidase 2 Regulates NLRP3 Inflammasome Activation in the Brain after Traumatic Brain Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Merry W. Ma ◽  
Jing Wang ◽  
Krishnan M. Dhandapani ◽  
Darrell W. Brann
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nadph Oxidase ◽  
Nlrp3 Inflammasome ◽  
Healing Process ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Nadph Oxidase 2

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. After the initial primary mechanical injury, a complex secondary injury cascade involving oxidative stress and neuroinflammation follows, which may exacerbate the injury and complicate the healing process. NADPH oxidase 2 (NOX2) is a major contributor to oxidative stress in TBI pathology, and inhibition of NOX2 is neuroprotective. The NLRP3 inflammasome can become activated in response to oxidative stress, but little is known about the role of NOX2 in regulating NLRP3 inflammasome activation following TBI. In this study, we utilized NOX2 knockout mice to study the role of NOX2 in mediating NLRP3 inflammasome expression and activation following a controlled cortical impact. Expression of NLRP3 inflammasome components NLRP3 and apoptosis-associated speck-like protein containing a CARD (ASC), as well as its downstream products cleaved caspase-1 and interleukin-1β (IL-1β), was robustly increased in the injured cerebral cortex following TBI. Deletion of NOX2 attenuated the expression, assembly, and activity of the NLRP3 inflammasome via a mechanism that was associated with TXNIP, a sensor of oxidative stress. The results support the notion that NOX2-dependent inflammasome activation contributes to TBI pathology.

NADPH oxidase 2 deletion enhances neurogenesis following traumatic brain injury

2018 ◽  
Vol 123 ◽  
pp. 62-71 ◽  
Author(s):  
Jing Wang ◽  
Merry W. Ma ◽  
Krishnan M. Dhandapani ◽  
Darrell W. Brann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nadph Oxidase ◽  
Nadph Oxidase 2

scholarly journals In vivo imaging of rapid deformation and strain in an animal model of traumatic brain injury

2006 ◽  
Vol 39 (6) ◽  
pp. 1086-1095 ◽  
Author(s):  
Philip V. Bayly ◽  
Erin E. Black ◽  
Rachel C. Pedersen ◽  
Elizabeth P. Leister ◽  
Guy M. Genin
Keyword(s):  
Traumatic Brain Injury ◽  
Animal Model ◽  
Brain Injury ◽  
In Vivo Imaging ◽  
Rapid Deformation

scholarly journals Effects of Veliparib on Microglial Activation and Functional Outcomes after Traumatic Brain Injury in the Rat and Pig

2018 ◽  
Vol 35 (7) ◽  
pp. 918-929 ◽  
Author(s):  
Karen-Amanda Irvine ◽  
Robin K. Bishop ◽  
Seok Joon Won ◽  
Jianguo Xu ◽  
Katherine A. Hamel ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcomes ◽  
Microglial Activation

scholarly journals Experimental model of intracranial hypertension with continuous multiparametric monitoring in swine

2013 ◽  
Vol 71 (10) ◽  
pp. 802-806 ◽  
Author(s):  
Almir Ferreira de Andrade ◽  
Matheus Schmidt Soares ◽  
Gustavo Cartaxo Patriota ◽  
Alessandro Rodrigo Belon ◽  
Wellingson Silva Paiva ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Animal Model ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Severe Traumatic Brain Injury ◽  
Transcranial Doppler ◽  
Porcine Model ◽  
Cerebral Oximetry ◽  
Suitable Animal Model

Objective Intracranial hypertension (IH) develops in approximately 50% of all patients with severe traumatic brain injury (TBI). Therefore, it is very important to identify a suitable animal model to study and understand the pathophysiology of refractory IH to develop effective treatments. Methods We describe a new experimental porcine model designed to simulate expansive brain hematoma causing IH. Under anesthesia, IH was simulated with a balloon insufflation. The IH variables were measured with intracranial pressure (ICP) parenchymal monitoring, epidural, cerebral oximetry, and transcranial Doppler (TCD). Results None of the animals died during the experiment. The ICP epidural showed a slower rise compared with parenchymal ICP. We found a correlation between ICP and cerebral oximetry. Conclusion The model described here seems useful to understand some of the pathophysiological characteristics of acute IH.

scholarly journals Neuroglobin Genetic Polymorphisms and Their Relationship to Functional Outcomes after Traumatic Brain Injury

2010 ◽  
Vol 27 (6) ◽  
pp. 999-1006 ◽  
Author(s):  
Pei-Ying Chuang ◽  
Yvette P. Conley ◽  
Samuel M. Poloyac ◽  
David O. Okonkwo ◽  
Dianxu Ren ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Genetic Polymorphisms ◽  
Functional Outcomes
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