scholarly journals Hypoxia preconditioning protects neuronal cells against traumatic brain injury through stimulation of glucose transport mediated by HIF-1α/GLUTs signaling pathway in rat

2020 ◽  
Author(s):  
Xiaogang Wu ◽  
Chunlin Wang ◽  
Jinbiao Wang ◽  
Meijie Zhu ◽  
Yinsheng Yao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Glucose Transport ◽  
Hypoxia Tolerance ◽  
Tunel Staining ◽  
Transport Activity ◽  
Neuroprotective Effects ◽  
Hypoxia Preconditioning ◽  
Cerebral Cortex Tissue

AbstractHypoxia preconditioning (HPC), a well-established preconditioning model, has been shown to protect the brain against severe hypoxia or ischemia caused by traumatic brain injury (TBI), but the mechanism has not been well elucidated. Anaerobic glycolysis is the major way for neurons to produce energy under cerebral ischemia and hypoxia after TBI, and it requires large amounts of glucose. We hypothesized that glucose transport, as a rate-limiting step of glucose metabolism, may play key roles in the neuroprotective effects of HPC on cerebral cortex tissue against TBI. The aim of this study was to investigate the effect of HPC on glucose transport activity of rat cerebral cortex tissue after TBI through examining the gene expression of two major glucose transporters (GLUT1 and GLUT3) and their upstream target gene hypoxia-inducible factor-1α (HIF-1α). Sprague-Dawley rats were treated with HPC (50.47 kPa, 3 h/d, 3d). Twenty-four hours after the last treatment, the rats were injured using the Feeney free falling model. Cortex tissues of injured rats were removed at 1 h, 4 h, 8 h, 12 h, 1 day, 3 days, 7 d, and 14 days post-injury for histological analysis. Compared with TBI alone, HPC before TBI resulted in the expression of HIF-1α, GLUT1, and GLUT3 to increase at 1 h; they were markedly increased at 4 h, 8 h, 12 h, 1 day, and 3 days and decreased thereafter (p < 0.05). HPC before TBI could improve neuronal survival in rats by examining NeuN staining and observing reduced apoptosis by examining TUNEL staining. The result showed that HPC before TBI could increase the expression of GLUT1 and GLUT3. And through double immunofluorescence staining for GLUT3 and NeuN, the results strongly suggest that HPC improved glucose transport activity of neurons in rats with TBI. In summary, our results further support that HPC can improve hypoxia tolerance and attenuate neuronal loss of cerebral cortex in rats after TBI. The mechanism is mainly related to the increase of glucose transport activity through inducing GLUT1 and GLUT3 expression through upregulating HIF-1α expression.

scholarly journals Neuroprotective effects of crude extract of Crataegus songarica on a rat model of traumatic brain injury

2022 ◽  
Vol 20 (2) ◽  
pp. 293-299
Author(s):  
Xueliang Gao ◽  
Zhao Wang ◽  
Peilei Jia ◽  
Yapeng Zhao ◽  
Kai Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rat Model ◽  
Brain Cortex ◽  
Neuronal Survival ◽  
Underlying Mechanism ◽  
Tunel Staining ◽  
Heme Oxygenase 1 ◽  
Nissl Staining ◽  
Neuroprotective Effects

Purpose: To investigate the protective effect of Crataegus songarica extract (CSCE) against traumatic brain injury (TBI) in rats, and the underlying mechanism of action. Methods: A rat model of TBI was established via tracheal intubation procedure, and the rats were treated with graded doses of CSCE. Neuronal survival was determined by Nissl staining, while neuronal apoptosis was measured using TUNEL-staining. Neurological impairments were determined based on neurological severity score (NSS). Results: Treatment of TBI rats with CSCE enhanced neuronal survival and decreased TUNEL-positive cell fraction in the brain cortex. The treatment prevented elevation of NSS and suppressed mRNA and protein expression levels of IL-6 and TNF-α in brain cortex. Moreover, CSCE treatment prevented TBI-mediated suppression of activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and attenuated hydrogen peroxide (H2O2) levels in TBI rat brain cortex. Treatment of TBI rats with CSCE down-regulated NF-κB expression, increased Nrf2 expression and up-regulated mRNA expressions of heme oxygenase 1 (HO-1) and quinine oxidoreductase 1 (NQO-1). Conclusion: These results suggest that CSCE prevents TBI-mediated reduction in neuronal survival and inhibits brain cortical neuronal death in rats. It improves NSS and inhibits inflammatory response via activation of Nrf2 pathway and targeting of NF-κB expression. Therefore, CSCE is a potential therapeutic agent for TBI.

scholarly journals Biomechanics of Traumatic Brain Injury: Influences of the Morphologic Heterogeneities of the Cerebral Cortex

2008 ◽  
Vol 36 (7) ◽  
pp. 1203-1215 ◽  
Author(s):  
R.J.H. Cloots ◽  
H.M.T. Gervaise ◽  
J.A.W. van Dommelen ◽  
M.G.D. Geers
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

Development of a de novo arteriovenous malformation after severe traumatic brain injury

2014 ◽  
Vol 14 (4) ◽  
pp. 418-420 ◽  
Author(s):  
Brandon A. Miller ◽  
David I. Bass ◽  
Joshua J. Chern
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Arteriovenous Malformation ◽  
Severe Traumatic Brain Injury ◽  
Arteriovenous Malformations ◽  
De Novo ◽  
First Report ◽  
Congenital Lesions

Arteriovenous malformations (AVMs) are typically considered congenital lesions, although there is growing evidence for de novo formation of these lesions as well. The authors present the case of an AVM in the same cerebral cortex that had been affected by a severe traumatic brain injury (TBI) more than 6 years earlier. To the best of the authors' knowledge, this is the first report attributing the formation of an AVM directly to TBI.

Neuroprotective effects of collagen matrix in rats after traumatic brain injury

2015 ◽  
Vol 33 (2) ◽  
pp. 95-104 ◽  
Author(s):  
Samuel S. Shin ◽  
Ramesh Grandhi ◽  
Jeremy Henchir ◽  
Hong Q. Yan ◽  
Stephen F. Badylak ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Collagen Matrix ◽  
Neuroprotective Effects

Temporal Lobe Syndromes

2020 ◽  
pp. 122-135
Author(s):  
Arpit Parmar ◽  
G. S. Kaloiya ◽  
Harsimarpreet Kaur
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Temporal Lobe ◽  
Cerebral Artery ◽  
Left Temporal Lobe ◽  
Temporal Lobes ◽  
Functional Aspects ◽  
The Common

Temporal lobes are one of the four major lobes of the cerebral cortex and perform a complex array of interrelated functions. They play an important role in various day-to-day functioning. The common pathologies leading to isolated temporal lobe dysfunction are infarction (of the middle cerebral artery), hemorrhage, seizures, tumors, encephalitis, and traumatic brain injury. Temporal lobe syndromes include a wide array of various neurological (Kluver-Bucy syndrome, Geschwind Gastaut syndrome, etc.), elementary (e.g., vertiginous syndromes, hallucinations, etc.), neuropsychiatric (e.g., anxiety, agitation, aggression, etc.), and cognitive (e.g., Korsakoff amnesia, cortical deafness, etc.) disorders. The presentation depends on a multitude of factors including involvement of dominant or non-dominant lobe. Left temporal lobe involvement usually leads to various forms of aphasia while right side involvement leads to more covert and varied syndromes. In this chapter, the authors discuss the anatomy of the temporal lobe, its functional aspects, and various syndromes of temporal lobe dysfunction.

Role of quetiapine in protection of neurodegeneration after traumatic brain injury

2019 ◽  
Vol 55 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Joseph A Morra ◽  
Adekola O Alao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Negative Symptoms ◽  
Memory Loss ◽  
Hospital Setting ◽  
Small Animal ◽  
Rehabilitation Unit ◽  
Neuroprotective Effects ◽  
Neurologic Deficits ◽  
Patients Experience

Objective Schizophrenia is a chronic psychotic disorder in which patients experience positive and negative symptoms for over six months. Schizophrenia is associated with early mortality, with 40% of this excess mortality due to suicide. This is a case of patient with schizophrenia who was treated with quetiapine after suffering a traumatic brain injury and recovered enough to be discharged to a rehabilitation unit. This case illustrates the neuroprotective effects of quetiapine in treating neurologic deficits in a patient who recently suffered a traumatic brain injury. Method This is a case report of a patient with schizophrenia treated in the hospital setting. He was placed on quetiapine after suffering a traumatic brain injury due to a suicide attempt in which he shot himself with a nail gun. Results The patient initially presented with neurologic deficits suggestive of traumatic brain injury (inattention, memory loss, muscle weakness) and psychosis from schizophrenia. He was treated with quetiapine and recovered enough to be discharged to a rehabilitation unit. Conclusion Quetiapine, a second-generation antipsychotic, has been shown to significantly decrease blood–brain barrier hyperpermeability by preserving tight junction integrity in small animal models. This anti-inflammatory effect may also help to preserve neurogenesis in patients with traumatic brain injury, as shown in this case. This case may help elucidate the nature of quetiapine’s neuroprotective effects in patients who have suffered traumatic brain injury and also highlights the need to further investigate other atypical antipsychotics and their potential neuroprotective role in treating traumatic brain injury.

Increased expression of ferritin in cerebral cortex after human traumatic brain injury

2012 ◽  
Vol 34 (7) ◽  
pp. 1173-1180 ◽  
Author(s):  
Huan-Dong Liu ◽  
Wei Li ◽  
Zhen-Rui Chen ◽  
Meng-Liang Zhou ◽  
Zong Zhuang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

scholarly journals Multiple Sites of Vasopressin Synthesis in the Injured Brain

2010 ◽  
Vol 31 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Brian J Zink ◽  
Adam Chodobski
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Impact Model ◽  
Proinflammatory Mediators ◽  
Injured Brain ◽  
Pathophysiological Role ◽  
Cerebrovascular Endothelium ◽  
Vasopressin Synthesis

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

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