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https://www.readbyqxmd.com/read/29774773/mir-711-induced-down-regulation-of-angiopoietin-1-mediates-neuronal-cell-death
#1
Boris Sabirzhanov, Alan Faden, Taryn Aubrecht, Rebecca Henry, Ethan Glaser, Bogdan A Stoica
Angiopoietin-1 (Ang-1) is a well-known endothelial growth factor but its effects on neurons have yet to be elucidated. We show that Ang-1 is rapidly down-regulated in the injured brain after controlled cortical impact (CCI), a mouse experimental TBI model and in etoposide-induced neuronal apoptosis in vitro. Ang-1 treatment inhibits etoposide-induced up-regulation of pro-apoptotic Bcl-2 family members Noxa, Puma, Bim, and Bax; reduces markers of caspase-dependent (cytochrome c release/caspase activation) and caspase-independent (apoptosis-inducing factor release) pathways; and limits neuronal cell death...
May 18, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29768967/interleukin-1-receptor-1-deletion-in-focal-and-diffuse-experimental-traumatic-brain-injury-in-mice
#2
Joon Yong Chung, Nicolas Krapp, Limin Wu, Sevda Lule, Lauren McAllister, William Edmiston Iii, Samantha Martin, Emily Levy, Tanya Songtachalert, John Sherwood, Erin Buckley, Bharat Sanders, Saef Izzy, Suzanne Hickman, Shuzhen Guo, Josephine Lok, Joseph El Khoury, Eng Lo, David Kaplan, Michael Whalen
Important differences in the biology of focal and diffuse traumatic brain injury (TBI) subtypes may result in unique pathophysiological responses to shared molecular mechanisms. Interleukin-1 (IL-1) signaling has been tested as a potential therapeutic target in preclinical models of cerebral contusion and diffuse TBI, and in a phase II clinical trial, but no published studies have examined IL-1 signaling in an impact/acceleration closed head injury (CHI) model. We hypothesized that genetic deletion of IL-1 receptor-1 (IL-1R1 KO) would be beneficial in focal (contusion) and CHI in mice...
May 17, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29742510/hmgb1-a-box-reverses-brain-edema-and-deterioration-of-neurological-function-in-a-traumatic-brain-injury-mouse-model
#3
Lijun Yang, Feng Wang, Liang Yang, Yunchao Yuan, Yan Chen, Gengshen Zhang, Zhenzeng Fan
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...
May 8, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29740274/inhibition-of-epac2-attenuates-neural-cell-apoptosis-and-improves-neurological-deficits-in-a-rat-model-of-traumatic-brain-injury
#4
Ling Zhang, Li Zhang, Huixiang Liu, Feng Jiang, Huanjing Wang, Di Li, Rong Gao
Traumatic brain injury (TBI) is a major cause of mortality and disability worldwide. TBI-induced neuronal apoptosis is one of the main contributors to the secondary injury process. The aim of this study is to investigate the involvement of Exchange protein directly activated by cAMP 2 (Epac2) on TBI. We found that the expression level of Epac2 surrounding the injured area of brain in rats of TBI model was significantly increased at 12 h after TBI. The role of Epac2 in TBI was further explored by using a selective Epac2 antagonist ESI-05 to decrease the Epac2 expression...
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29737232/kir6-2-the-pore-forming-subunit-of-atp-sensitive-k-channels-is-overexpressed-in-human-post-traumatic-brain-contusions
#5
Lidia Castro, Montoya Noelia, Marian Vidal-Jorge, David Sanchez-Ortiz, Dario Gándara, Elena Martínez-Saez, Marta Cicuendez, Maria A Poca, J Marc Simard, Juan Sahuquillo
Brain contusions (BCs) are one of the most frequent lesions in patients with moderate and severe traumatic brain injury (TBI). BCs increase their volume due to perilesional edema formation and/or hemorrhagic transformation. This may have deleterious consequences and its mechanisms are still poorly understood. We previously identified de novo upregulation SUR1, the regulatory subunit of KATP and other channels, in human BCs. Our aim here was to study the expression of the pore-forming subunit of KATP, Kir6.2, in human BCs, and identify its localization in different cell types...
May 8, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29730418/effects-of-pregabalin-on-brain-edema-neurologic-and-histologic-outcomes-in-experimental-traumatic-brain-injury
#6
Manzumeh-Shamsi Meymandi, Zahra Soltani, Gholamreza Sepehri, Sedigheh Amiresmaili, Fatemeh Farahani, Mohammadmehdi Moeini Aghtaei
Brain edema and increased intracranial pressure (ICP) are among the main causes of neurological disturbance and mortality following traumatic brain injury (TBI). Since pregabalin neuroprotective effects have been shown, this study was performed to evaluate the possible neuroprotective effects of pregabalin in experimental TBI of male rats. Adult male Wistar rats were divided into 4 groups: sham, vehicle, pregabalin 30 mg/kg and pregabalin 60 mg/kg. TBI was induced in vehicle and pregabalin groups by Marmarou method...
May 3, 2018: Brain Research Bulletin
https://www.readbyqxmd.com/read/29719500/valproic-acid-attenuates-traumatic-brain-injury-induced-inflammation-in-vivo-involvement-of-autophagy-and-the-nrf2-are-signaling-pathway
#7
Xiangrong Chen, Handong Wang, Mengliang Zhou, Xiang Li, Zhongning Fang, Hongzhi Gao, Yasong Li, Weipeng Hu
Microglial activation and the inflammatory response in the central nervous system (CNS) play important roles in secondary damage after traumatic brain injury (TBI). Transcriptional activation of genes that limit secondary damage to the CNS are mediated by a cis-acting element called the antioxidant responsive element (ARE). ARE is known to associate with the transcription factor NF-E2-related factor 2 (Nrf2), a transcription factor that is associated with histone deacetylases (HDACs). This pathway, known as the Nrf2/ARE pathway, is a critical antioxidative factor pathway that regulates the balance of oxygen free radicals and the inflammatory response, and is also related to autophagic activities...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29714150/cinnamon-polyphenol-extract-exerts-neuroprotective-activity-in-traumatic-brain-injury-through-modulation-of-nfr2-and-cytokine-expression
#8
Burak Yulug, Ertugrul Kilic, Serdar Altunay, Cenk Ersavas, Cemal Orhan, Arman Dalay, Nurhan Sahin, Mehmet Tuzcu, Vijaya Juturu, Kazim Sahin
INTRODUCTION: Cinnamon cinnamon polyphenol extract is a traditional spice commonly used in different areas of the world for treatment of different disease conditions which are associated with inflammation and oxidative stress. Despite many preclinical studies showing the anti-oxidative, anti-inflammatory effects of CN, the underlying mechanisms in signaling pathways via which cinnamon protects the brain after brain trauma remained largely unknown. However, there is still no preclinical study delineating the possible molecular mechanism of neuroprotective effects cinnamon polyphenol extractin TBI...
April 30, 2018: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/29698747/neuroprotective-effects-of-metformin-on-traumatic-brain-injury-in-rats-associated-with-nf-%C3%AE%C2%BAb-and-mapk-signaling-pathway
#9
Li Tao, Di Li, Huixiang Liu, Feng Jiang, Yitian Xu, Gang Chen, Ying Cao, Rong Gao
Traumatic brain injury (TBI) triggers a complex sequence of inflammatory responses that contribute to secondary injury. Metformin, a first-line drug used to treat type 2 diabetes, is reported to exhibit potent anti-inflammatory activity on diseases associated with the central nervous system (CNS). The aim of this study is to investigate the potential neuroprotective effects of metformin on acute brain injury after TBI and explore the underlying mechanisms. Male Sprague-Dawley (SD) rats were divided into four groups: sham group, TBI group, TBI + saline (NS) group and TBI + metformin group...
April 23, 2018: Brain Research Bulletin
https://www.readbyqxmd.com/read/29693126/neuroprotective-effects-of-dexmedetomidine-on-traumatic-brain-injury-involvement-of-neuronal-apoptosis-and-hsp70-expression
#10
Man-He Zhang, Xiu-Min Zhou, Jian-Zhong Cui, Kai-Jie Wang, Yan Feng, Hong-Ao Zhang
The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in the hippocampus. A total of 90 adult male Sprague‑Dawley rats were randomly assigned into 3 groups (n=30/group): Sham, TBI and Dex groups. The rat models of TBI were established using a modified weight‑drop device and Dex (15 µg/kg) was intravenously administered immediately following TBI...
April 19, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29669346/tetrahydrocurcumin-provides-neuroprotection-in-experimental-traumatic-brain-injury-and-the-nrf2-signaling-pathway-as-a-potential-mechanism
#11
Guan Wei, Bingji Chen, Qingjiang Lin, Yasong Li, Liangqin Luo, Hefan He, Huangde Fu
The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood. This study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group...
April 18, 2018: Neuroimmunomodulation
https://www.readbyqxmd.com/read/29665077/gliovascular-changes-precede-white-matter-damage-and-long-term-disorders-in-juvenile-mild-closed-head-injury
#12
Beatriz Rodriguez-Grande, Andre Obenaus, Aleksandra Ichkova, Justine Aussudre, Thomas Bessy, Elodie Barse, Bassem Hiba, Gwénaëlle Catheline, Grégory Barrière, Jerome Badaut
Traumatic brain injury (TBI) is a leading cause of hospital visits in pediatric patients and often leads to long-term disorders even in cases of mild severity. White matter (WM) alterations are commonly observed in patients months or years after the injury assessed by magnetic resonance imaging (MRI), but little is known about WM pathophysiology early after mild pediatric TBI. To evaluate the status of the gliovascular unit in this context, mild TBI was induced in postnatal-day 17 mice using a closed head injury model with two grades of severity (G1, G2)...
April 17, 2018: Glia
https://www.readbyqxmd.com/read/29648981/glibenclamide-produces-region-dependent-effects-on-cerebral-edema-in-a-combined-injury-model-of-traumatic-brain-injury-and-hemorrhagic-shock-in-mice
#13
Ruchira Jha, Bradley J Molyneaux, Travis C Jackson, Jessica Wallisch, Seo-Young Park, Samuel M Poloyac, Vincent A Vagni, Keri L Janesko-Feldman, Keito Hoshitsuki, Margaret Beth Minnigh, Patrick M Kochanek
Cerebral edema is critical to morbidity/mortality in TBI and is worsened by hypotension. Glibenclamide may reduce cerebral edema by inhibiting sulfonylurea receptor-1 (Sur1); its effect on diffuse cerebral edema exacerbated by hypotension/resuscitation is unknown. We aimed to determine if glibenclamide improves pericontusional and/or diffuse edema in controlled cortical impact (CCI, 5m/s, 1 mm-depth)+hemorrhagic shock (HS, 35 minutes), and compare its effects in CCI alone. C57/BL6 mice were divided into 5 groups (n=10/group): naïve, CCI+vehicle, CCI+glibenclamide, CCI+HS+vehicle, and CCI+HS+glibenclamide...
March 8, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29648978/fgf21-protects-the-blood-brain-barrier-by-upregulating-ppar%C3%AE-via-fgfr1-%C3%AE-klotho-following-traumatic-brain-injury
#14
Jun Chen, Jian Hu, Huan Liu, Ye Xiong, Yuchi Zou, Wenting Huang, Mingjie Shao, Jiamin Wu, Li Yu, Xiaojie Wang, Xue Wang, Li Lin
Blood-brain barrier (BBB) disruption and dysfunction result in brain edema, which is responsible for more than half of all deaths after severe traumatic brain injury (TBI). Fibroblast growth factor 21 (FGF21) has a potential neuroprotective function in the brain. However, the effects and underlying possible mechanism of action on BBB integrity following TBI remain unknown. The purpose of the current study was to determine the effects of FGF21 on BBB protection and TBI treatment. The effects of recombinant human FGF21 (rhFGF21) on BBB integrity and on tight junction and adherens junction proteins were investigated both in a TBI mouse model and an in vitro BBB disruption model established with TNF-α-induced human brain microvascular endothelial cells (HBMECs)...
March 6, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29620218/quercetin-protects-rat-cortical-neurons-against-traumatic-brain-injury
#15
Guoliang Du, Zongmao Zhao, Yonghan Chen, Zonghao Li, Yaohui Tian, Zhifeng Liu, Bin Liu, Jianqiang Song
Previous studies have demonstrated that traumatic brain injury (TBI) may cause neurological deficits and neuronal cell apoptosis. Quercetin, one of the most widely distributed flavonoids, possesses anti‑inflammatory, anti‑blood coagulation, anti‑ischemic and anti‑cancer activities, and neuroprotective effects in the context of brain injury. The purpose of the present study was to investigate the neuroprotective effects of quercetin in TBI. A total of 75 rats were randomly arranged into 3 groups as follows: Sham group (Sham); TBI group (TBI); and TBI + quercetin group (Que)...
March 28, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29606856/sevoflurane-post-conditioning-attenuates-traumatic-brain-injury-induced-neuronal-apoptosis-by-promoting-autophagy-via-the-pi3k-akt-signaling-pathway
#16
Hefan He, Weifeng Liu, Yingying Zhou, Yibin Liu, Peiqing Weng, Yasong Li, Huangde Fu
Background: Sevoflurane post-conditioning exerts nerve-protective effects through inhibiting caspase-dependent neuronal apoptosis after a traumatic brain injury (TBI). Autophagy that is induced by the endoplasmic reticulum stress plays an important role in the secondary neurological dysfunction after a TBI. However, the relationship between autophagy and caspase-dependent apoptosis as well as the underlying nerve protection mechanism that occurs with sevoflurane post-conditioning following a TBI remains unclear...
2018: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/29600800/hypertonic-saline-alleviates-brain-edema-after-traumatic-brain-injury-via-downregulation-of-aquaporin-4-in-rats
#17
Jian Yin, Haixiao Zhang, Huai Chen, Qingping Lv, Xuhong Jin
BACKGROUND Hypertonic saline (HS) has been successfully used for treatment of various forms of brain edema. Decreased expression of aquaporin (AQP)4 and pro-inflammatory cytokines such as tumor necrosis factor (TNF)-a and interleukin (IL)-1b have been linked to edema pathogenesis. This study examined the effect of 3% HS on brain edema in a rat model of traumatic brain injury (TBI). MATERIAL AND METHODS Sprague-Dawley rats were subjected to TBI induced by a controlled cortical impactor. The HS group was injected with 3% NaCl until the end of the study period...
March 30, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29576714/rhubarb-attenuates-cerebral-edema-via-inhibition-of-the-extracellular-signal-regulated-kinase-pathway-following-traumatic-brain-injury-in-rats
#18
Zhaoyu Yang, Rong Fan, Peng Sun, Hanjin Cui, Weijun Peng, Jiekun Luo, Chunhu Zhang, Xingui Xiong, Wei Huang, Wei Liu
Background: Rhubarb is a traditional Chinese medicine for treating traumatic brain injury (TBI). Purpose: The purpose of this study is to elucidate the potential mechanism of rhubarb by suppressing extracellular signal-regulated kinase (ERK) to ameliorate brain edema. Materials and Methods: Sprague-Dawley rats were separated into four groups at random. One group received 3 g/kg rhubarb, and another group received 12 g/kg rhubarb, and the vehicle group and sham group were administered the same dose of saline solution...
January 2018: Pharmacognosy Magazine
https://www.readbyqxmd.com/read/29571711/curcumin-plays-neuroprotective-roles-against-traumatic-brain-injury-partly-via-nrf2-signaling
#19
Wenwen Dong, Bei Yang, Linlin Wang, Bingxuan Li, Xiangshen Guo, Miao Zhang, Zhenfei Jiang, Jingqi Fu, Jingbo Pi, Dawei Guan, Rui Zhao
Traumatic brain injury (TBI), which leads to high mortality and morbidity, is a prominent public health problem worldwide with no effective treatment. Curcumin has been shown to be beneficial for neuroprotection in vivo and in vitro, but the underlying mechanism remains unclear. This study determined whether the neuroprotective role of curcumin in mouse TBI is dependent on the NF-E2-related factor (Nrf2) pathway. The Feeney weight-drop contusion model was used to mimic TBI. Curcumin was administered intraperitoneally 15 min after TBI induction, and brains were collected at 24 h after TBI...
March 20, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29569703/histopathological-changes-in-the-choroid-plexus-after-traumatic-brain-injury-in-the-rats-a-histologic-and-immunohistochemical-study
#20
Hüseyin Özevren, Engin Deveci, Mehmet Cudi Tuncer
Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analyzed the histopathological changes in E-cadherin and VEGF expression after traumatic brain injury in rats. The rats were divided into 2 groups as the control and the trauma groups. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g⁻¹ m weight-height impact. After 5 days of traumatic brain injury, blood samples were taken under ketamine hydroxide anesthesia and biochemical analyzes were performed...
March 23, 2018: Folia Morphologica (Warsz)
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