scholarly journals Prognostic significance of translocator protein in the brain tissue following traumatic brain injury

2021 ◽  
Author(s):  
Qing Bao ◽  
Xuesong Yuan ◽  
Xiaoxing Bian ◽  
Wenfeng Wei ◽  
Peng Jin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Brain Tissue ◽  
Characteristic Curve ◽  
Prognostic Significance ◽  
Translocator Protein ◽  
Specificity And Sensitivity ◽  
Unit Increase ◽  
The Brain

Abstract Background The study aimed to measure the expression of translocator protein (TSPO) in brain tissue following traumatic brain injury (TBI) and to determine whether TSPO can predict outcomes. Methods TBI patients requiring emergent craniectomy and removing of intracranial hematoma were recruited from Wujin Hospital Affiliated with Jiangsu University between January 2018 and May 2020. TBI patients were divided into unfavorable and favorable groups according to GOS score. The TSPO in brain samples was analyzed by western blot and immunocytochemistry. Results The western blot and immunocytochemistry showed that the TSPO in the unfavorable group was higher than that in the favorable group. Double immunofluorescence staining exhibited that the percentage of TSPO positive cells in IBA1 and GFAP positive cells was 45.2 ± 3.1% and 3.5 ± 0.6% respectively. After adjusting for age, sex, CT, ICP and GCS, we found each 1-unit increase in TSPO was associated with 40% higher occurrence of unfavorable outcome (OR = 1.4, 95% CI 0.4–5.6). The area under the receiver operating characteristic curve (AUC), specificity, and sensitivity of TSPO was 0.87, 76.7%, 88.2% respectively. Conclusion Our study demonstrated that higher TSPO was associated with higher occurrence of unfavorable outcomes.

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.

scholarly journals Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Target Genes ◽  
Neural Function ◽  
Stress Genes ◽  
Expression Of Genes ◽  
Delayed Recovery ◽  
The Brain ◽  
Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

scholarly journals Embedded axonal fiber tracts improve finite element model predictions of traumatic brain injury

2019 ◽  
Vol 19 (3) ◽  
pp. 1109-1130 ◽  
Author(s):  
Marzieh Hajiaghamemar ◽  
Taotao Wu ◽  
Matthew B. Panzer ◽  
Susan S. Margulies
Keyword(s):  
Traumatic Brain Injury ◽  
Finite Element ◽  
Brain Injury ◽  
Strain Rate ◽  
Brain Tissue ◽  
Brain Injuries ◽  
Characteristic Curve ◽  
Strain And Strain Rate

AbstractWith the growing rate of traumatic brain injury (TBI), there is an increasing interest in validated tools to predict and prevent brain injuries. Finite element models (FEM) are valuable tools to estimate tissue responses, predict probability of TBI, and guide the development of safety equipment. In this study, we developed and validated an anisotropic pig brain multi-scale FEM by explicitly embedding the axonal tract structures and utilized the model to simulate experimental TBI in piglets undergoing dynamic head rotations. Binary logistic regression, survival analysis with Weibull distribution, and receiver operating characteristic curve analysis, coupled with repeated k-fold cross-validation technique, were used to examine 12 FEM-derived metrics related to axonal/brain tissue strain and strain rate for predicting the presence or absence of traumatic axonal injury (TAI). All 12 metrics performed well in predicting of TAI with prediction accuracy rate of 73–90%. The axonal-based metrics outperformed their rival brain tissue-based metrics in predicting TAI. The best predictors of TAI were maximum axonal strain times strain rate (MASxSR) and its corresponding optimal fraction-based metric (AF-MASxSR7.5) that represents the fraction of axonal fibers exceeding MASxSR of 7.5 s−1. The thresholds compare favorably with tissue tolerances found in in–vitro/in–vivo measurements in the literature. In addition, the damaged volume fractions (DVF) predicted using the axonal-based metrics, especially MASxSR (DVF = 0.05–4.5%), were closer to the actual DVF obtained from histopathology (AIV = 0.02–1.65%) in comparison with the DVF predicted using the brain-related metrics (DVF = 0.11–41.2%). The methods and the results from this study can be used to improve model prediction of TBI in humans.

Protective effects of quercetin on traumatic brain injury induced inflammation and oxidative stress in cortex through activating Nrf2/HO-1 pathway

2021 ◽  
Vol 39 (1) ◽  
pp. 73-84
Author(s):  
Jianqiang Song ◽  
Guoliang Du ◽  
Haiyun Wu ◽  
Xiangliang Gao ◽  
Zhen Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
The Brain ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. Objective: This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons. Methods: A modified weight-drop device was used for the TBI model. 5, 20 or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12 and 24 h post TBI. Rats were sacrificed three days post injury and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Results: Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats. Conclusions: Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.

scholarly journals Decompressive craniectomy of post-traumatic brain injury: an in silico modelling approach for intracranial hypertension management

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chryso Lambride ◽  
Nicolas Christodoulou ◽  
Anna Michail ◽  
Vasileios Vavourakis ◽  
Triantafyllos Stylianopoulos
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Brain Tissue ◽  
Decompressive Craniectomy ◽  
In Silico ◽  
Pressure Loading ◽  
Post Traumatic ◽  
The Brain

Abstract Traumatic brain injury (TBI) causes brain edema that induces increased intracranial pressure and decreased cerebral perfusion. Decompressive craniectomy has been recommended as a surgical procedure for the management of swollen brain and intracranial hypertension. Proper location and size of a decompressive craniectomy, however, remain controversial and no clinical guidelines are available. Mathematical and computational (in silico) models can predict the optimum geometric conditions and provide insights for the brain mechanical response following a decompressive craniectomy. In this work, we present a finite element model of post-traumatic brain injury and decompressive craniectomy that incorporates a biphasic, nonlinear biomechanical model of the brain. A homogenous pressure is applied in the brain to represent the intracranial pressure loading caused by the tissue swelling and the models calculate the deformations and stresses in the brain as well as the herniated volume of the brain tissue that exits the skull following craniectomy. Simulations for different craniectomy geometries (unilateral, bifrontal and bifrontal with midline bar) and sizes are employed to identify optimal clinical conditions of decompressive craniectomy. The reported results for the herniated volume of the brain tissue as a function of the intracranial pressure loading under a specific geometry and size of craniectomy are exceptionally relevant for decompressive craniectomy planning.

scholarly journals Analysis of the Histopathology, TNF-α of Microglia Cells Expression, NRG-1/erbB Oligodendrocyte, and Ki67/Apoptosis of Dentate Gyrus Rattus novergicus Brain After Acute Traumatic Brain Injury

2017 ◽  
Vol 6 (1) ◽  
pp. 20
Author(s):  
Wibi Riawan ◽  
Putri Fitri Alfiantya ◽  
Oktavia Rahayu Adianingsih ◽  
Zulkarnaen Zulkarnaen ◽  
Alif Fariz Jazmi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dentate Gyrus ◽  
Brain Tissue ◽  
Microscopic Observation ◽  
Pyramidal Cells ◽  
Adult Brain ◽  
Sprague Dawley ◽  
Tnf Α ◽  
The Brain

Head trauma or traumatic brain injury (TBI) gives most serious impact on the central nervous system. Several experimental models have been established to mimic different pathogenesis characteristics of TBI. The purpose of this study was to determine whether there is evidence of hystopathological lesions in the brain tissue after Marmorou TBI models. This study uses Rattus norvegicus Sprague Dawley strain. Macroscopic and microscopic observations on the brain tissue were done. Macroscopic lesions were observed in the brain. Microscopic observation was performed with Haematoxylin-Eosin (HE) staining and immunohistochemistry on the distribution of microglia cells and pyramidal cells in the cortex. Meanwhile, the distribution of NRG-1/ErbB, proliferation, and apoptosis were observed in the hippocampus. The results of macroscopic observation showed that there were wounds caused by falling loads and vasodilatation. On microscopic observation, the TBI group showed an increase in neutrophils distribution and distribution of activated microglia to produce TNF-α, and decrease in the number of cortical pyramidal cells significantly. The distribution of NRG-1 tended to decrease after exposure of TBI and had no effect on its receptor, erbB. Exposure of TBI appears to lower the activity of neuronal cells proliferation in dentate gyrus (DG) area and significantly increase the number of apoptotic cells. Marmarou model is a physiological model of TBI that spontaneously occurs following a trauma to the head, for example trauma due to an accident. This data can be used as a preliminary data of inflammation and tissue regeneration of disrupted adult brain. Therefore, this research could be used as the basis in the studies of therapeutic agents in the process of neurogenesis of brain cells.Keywords: traumatic brain injury, ERG-1/ErbB, dentate gyrus, Ki67, TNF-a, microglia

scholarly journals Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Einars Kupats ◽  
Gundega Stelfa ◽  
Baiba Zvejniece ◽  
Solveiga Grinberga ◽  
Edijs Vavers ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Aminobutyric Acid ◽  
Drug Candidate ◽  
H2o2 Production ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
The Impact ◽  
The Brain

Altered neuronal Ca2+ homeostasis and mitochondrial dysfunction play a central role in the pathogenesis of traumatic brain injury (TBI). R-Phenibut ((3R)-phenyl-4-aminobutyric acid) is an antagonist of the α2δ subunit of voltage-dependent calcium channels (VDCC) and an agonist of gamma-aminobutyric acid B (GABA-B) receptors. The aim of this study was to evaluate the potential therapeutic effects of R-phenibut following the lateral fluid percussion injury (latFPI) model of TBI in mice and the impact of R- and S-phenibut on mitochondrial functionality in vitro. By determining the bioavailability of R-phenibut in the mouse brain tissue and plasma, we found that R-phenibut (50 mg/kg) reached the brain tissue 15 min after intraperitoneal (i.p.) and peroral (p.o.) injections. The maximal concentration of R-phenibut in the brain tissues was 0.6 μg/g and 0.2 μg/g tissue after i.p. and p.o. administration, respectively. Male Swiss-Webster mice received i.p. injections of R-phenibut at doses of 10 or 50 mg/kg 2 h after TBI and then once daily for 7 days. R-Phenibut treatment at the dose of 50 mg/kg significantly ameliorated functional deficits after TBI on postinjury days 1, 4, and 7. Seven days after TBI, the number of Nissl-stained dark neurons (N-DNs) and interleukin-1beta (IL-1β) expression in the cerebral neocortex in the area of cortical impact were reduced. Moreover, the addition of R- and S-phenibut at a concentration of 0.5 μg/ml inhibited calcium-induced mitochondrial swelling in the brain homogenate and prevented anoxia-reoxygenation-induced increases in mitochondrial H2O2 production and the H2O2/O ratio. Taken together, these results suggest that R-phenibut could serve as a neuroprotective agent and promising drug candidate for treating TBI.

Prognostic significance of serum translocator protein in patients with traumatic brain injury

2019 ◽  
Vol 488 ◽  
pp. 25-30 ◽  
Author(s):  
Li-Feng Luo ◽  
Jian-Feng Weng ◽  
Meng Cen ◽  
Xiao-Qiao Dong ◽  
Wen-Hua Yu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Prognostic Significance ◽  
Translocator Protein

New Insights into Oxidative Damage and Iron Associated Impairment in Traumatic Brain Injury

2020 ◽  
Vol 25 (45) ◽  
pp. 4737-4746
Author(s):  
Nicolas Toro-Urrego ◽  
Liliana F. Turner ◽  
Marco F. Avila-Rodriguez
Keyword(s):  
Reactive Oxygen Species ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Brain Tissue ◽  
Reactive Oxygen ◽  
Iron Chelators ◽  
Oxygen Species ◽  
Underlying Mechanisms ◽  
The Brain

: Traumatic Brain Injury is considered one of the most prevalent causes of death around the world; more than seventy millions of individuals sustain the condition per year. The consequences of traumatic brain injury on brain tissue are complex and multifactorial, hence, the current palliative treatments are limited to improve patients’ quality of life. The subsequent hemorrhage caused by trauma and the ongoing oxidative process generated by biochemical disturbances in the in the brain tissue may increase iron levels and reactive oxygen species. The relationship between oxidative damage and the traumatic brain injury is well known, for that reason, diminishing factors that potentiate the production of reactive oxygen species have a promissory therapeutic use. Iron chelators are molecules capable of scavenging the oxidative damage from the brain tissue and are currently in use for ironoverload- derived diseases. : Here, we show an updated overview of the underlying mechanisms of the oxidative damage after traumatic brain injury. Later, we introduced the potential use of iron chelators as neuroprotective compounds for traumatic brain injury, highlighting the action mechanisms of iron chelators and their current clinical applications.

Sign in / Sign up

Export Citation Format

Share Document