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https://www.readbyqxmd.com/read/28912751/decreased-secondary-lesion-growth-and-attenuated-immune-response-after-traumatic-brain-injury-in-tlr2-4-mice
#1
Sandro M Krieg, Florian Voigt, Pascal Knuefermann, Carsten Jürgen Kirschning, Nikolaus Plesnila, Florian Ringel
Danger-associated molecular patterns are released by damaged cells and trigger neuroinflammation through activation of non-specific pattern recognition receptors, e.g., toll-like receptors (TLRs). Since the role of TLR2 and 4 after traumatic brain injury (TBI) is still unclear, we examined the outcome and the expression of pro-inflammatory mediators after experimental TBI in Tlr2/4(-/-) and wild-type (WT) mice. Tlr2/4(-/-) and WT mice were subjected to controlled cortical injury and contusion volume and brain edema formation were assessed 24 h thereafter...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28905273/early-to-long-term-alterations-of-cns-barriers-after-traumatic-brain-injury-considerations-for-drug-development
#2
Beatriz Rodriguez-Grande, Aleksandra Ichkova, Sighild Lemarchant, Jerome Badaut
Traumatic brain injury (TBI) is one of the leading causes of death and disability, particularly amongst the young and the elderly. The functions of the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) are strongly impaired after TBI, thus affecting brain homeostasis. Following the primary mechanical injury that characterizes TBI, a secondary injury develops over time, including events such as edema formation, oxidative stress, neuroinflammation, and alterations in paracelullar and transcellular transport...
September 13, 2017: AAPS Journal
https://www.readbyqxmd.com/read/28856566/cold-environment-exacerbates-brain-pathology-and-oxidative-stress-following-traumatic-brain-injuries-potential-therapeutic-effects-of-nanowired-antioxidant-compound-h-290-51
#3
Aruna Sharma, Dafin F Muresanu, José Vicente Lafuente, Per-Ove Sjöquist, Ranjana Patnaik, Z Ryan Tian, Asya Ozkizilcik, Hari S Sharma
The possibility that traumatic brain injury (TBI) occurring in a cold environment exacerbates brain pathology and oxidative stress was examined in our rat model. TBI was inflicted by making a longitudinal incision into the right parietal cerebral cortex (2 mm deep and 4 mm long) in cold-acclimatized rats (5 °C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in cold-exposed rats exhibited pronounced increase in brain lucigenin (LCG), luminol (LUM), and malondialdehyde (MDA) and marked pronounced decrease in glutathione (GTH) as compared to identical TBI at room temperature...
August 30, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28836291/introducing-the-concept-of-csf-shift-edema-in-traumatic-brain-injury
#4
REVIEW
Iype Cherian, Margarita Beltran, Alessandro Landi, Concetta Alafaci, Fabio Torregrossa, Giovanni Grasso
Brain edema after severe traumatic brain injury (TBI) plays an important role in the outcome and survival of injured patients. It is also one of the main targets in the therapeutic approach in the current clinical practice. To date, the pathophysiology of traumatic brain swelling is complex and, being that it is thought to be mainly cytotoxic and vasogenic in origin, not yet entirely understood. However, based on new understandings of the hydrodynamic aspects of cerebrospinal fluid (CSF), an additional mechanism of brain swelling can be considered...
August 24, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28835703/neuroprotective-effects-of-cgp3466b-on-apoptosis-are-modulated-by-protein-l-isoaspartate-d-aspartate-o-methyltransferase-mst1-pathways-after-traumatic-brain-injury-in-rats
#5
Feng Liang, Ligen Shi, Jingwei Zheng, Sheng Chen, Yangxin Wang, Jianmin Zhang
Neuronal apoptosis chiefly contributes to the cell loss following traumatic brain injury (TBI). CGP3466B is a compound related to the anti-Parkinsonism drug R-(-)-deprenyl. Previous studies have illuminated anti-apoptosis effects of CGP3466B in different cell lines, but the underlying mechanisms have not been fully elucidated. Mammalian sterile 20 (STE20)-like kinase1 (Mst1) is a core component of the Hippo signaling pathway. Protein-L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) is an enzyme that repairs damaged L-isoaspartyl residues in proteins...
August 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28812113/-pathophysiology-of-intracranial-injuries
#6
REVIEW
D Lahner, G Fritsch
Traumatic brain injury (TBI) constitutes a heterogeneous condition that affects the most complex organ of the human body. It is commonly classified by its location as focal injury (e.g. epidural hematoma) and diffuse injury (e.g. diffuse axonal shearing injury) as well as by primary and secondary tissue injury. Accordingly, direct mechanical force causes the primary insult. The tissue damage occurring afterwards is subsumed under the term secondary brain damage. Some of these processes are overlapping and include in the early phase local cerebral ischemia resulting in excitotoxicity, which together with the triggered neuroinflammatory cascade causes the formation of cerebral edema and ultimately increased intracranial pressure once the intracranial compliance is exhausted...
August 15, 2017: Der Unfallchirurg
https://www.readbyqxmd.com/read/28782716/treatment-with-an-interleukin-1-receptor-antagonist-mitigates-neuroinflammation-and-brain-damage-after-polytrauma
#7
Mujun Sun, Rhys D Brady, David K Wright, Hyun Ah Kim, Shenpeng R Zhang, Christopher G Sobey, Maddison R Johnstone, Terence J O'Brien, Bridgette D Semple, Stuart J McDonald, Sandy R Shultz
Traumatic brain injury (TBI) and long bone fracture are common in polytrauma. This injury combination in mice results in elevated levels of the pro-inflammatory cytokine interleukin-1β (IL-1β) and exacerbated neuropathology when compared to isolated-TBI. Here we examined the effect of treatment with an IL-1 receptor antagonist (IL-1ra) in mice given a TBI and a concomitant tibial fracture (i.e., polytrauma). Adult male C57BL/6 mice were given sham-injuries or polytrauma and treated with saline-vehicle or IL-1ra (100 mg/kg)...
August 3, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28770828/sesamin-alleviates-blood-brain-barrier-disruption-in-mice-with-experimental-traumatic-brain-injury
#8
Ying-Liang Liu, Zhi-Ming Xu, Guo-Yuan Yang, Dian-Xu Yang, Jun Ding, Hao Chen, Fang Yuan, Heng-Li Tian
Sesamin, a major lignan of sesame oil, was reported to have neuroprotective effects in several brain injury models. However, its protective action in maintaining blood-brain barrier (BBB) integrity has not been studied. In this study we investigated the effects of sesamin on the BBB in a mouse model of traumatic brain injury (TBI) and explored the underlying mechanisms. Adult male C57BL/6 mice were subjected to a controlled cortical impact (CCI) injury and then received sesamin (30 mg·kg(-1)·d(-1), ip). The mice were euthanized on the 1(st) and 3(rd) days after CCI injury and samples were collected for analysis...
August 3, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28759166/altered-metabolites-of-the-rat-hippocampus-after-mild-and-moderate-traumatic-brain-injury-a-combined-in-vivo-and-in-vitro-1-h-mrs-study
#9
Kavita Singh, Richa Trivedi, Ajay Verma, Maria M D'souza, Sunil Koundal, Poonam Rana, Bikash Baishya, Subash Khushu
Traumatic brain injury (TBI) has been shown to affect hippocampus-associated learning, memory and higher cognitive functions, which may be a consequence of metabolic alterations. Hippocampus-associated disorders may vary depending on the severity of injury [mild TBI (miTBI) and moderate TBI (moTBI)] and time since injury. The underlying hippocampal metabolic irregularities may provide an insight into the pathological process following TBI. In this study, in vivo and in vitro proton magnetic resonance spectroscopy ((1) H-MRS) data were acquired from the hippocampus region of controls and TBI groups (miTBI and moTBI) at D0 (pre-injury), 4 h, Day 1 and Day 5 post-injury (PI)...
July 31, 2017: NMR in Biomedicine
https://www.readbyqxmd.com/read/28754973/neuroprotective-effects-of-trigeminal-nerve-stimulation-in-severe-traumatic-brain-injury
#10
Amrit Chiluwal, Raj K Narayan, Wayne Chaung, Neal Mehan, Ping Wang, Chad E Bouton, Eugene V Golanov, Chunyan Li
Following traumatic brain injury (TBI), ischemia and hypoxia play a major role in further worsening of the damage, a process referred to as 'secondary injury'. Protecting neurons from causative factors of secondary injury has been the guiding principle of modern TBI management. Stimulation of trigeminal nerve induces pressor response and improves cerebral blood flow (CBF) by activating the rostral ventrolateral medulla. Moreover, it causes cerebrovasodilation through the trigemino-cerebrovascular system and trigemino-parasympathetic reflex...
July 28, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28751738/apoe-influences-the-blood-brain-barrier-through-the-nf-%C3%AE%C2%BAb-mmp-9-pathway-after-traumatic-brain-injury
#11
Zhipeng Teng, Zongduo Guo, Jianjun Zhong, Chongjie Cheng, Zhijian Huang, Yue Wu, Shuang Tang, Chao Luo, Xing Peng, Haitao Wu, Xiaochuan Sun, Li Jiang
Apolipoprotein E (ApoE), encoded by the ApoE gene (APOE), influences the outcomes of traumatic brain injury (TBI), but the mechanism remains unclear. The present study aimed to investigate the effects of different ApoEs on the outcome of TBI and to explore the possible mechanisms. Controlled cortical impact (CCI) was performed on APOEε3 (E3) and APOEε4 (E4) transgenic mice, APOE-KO (KO) mice, and wild type (WT) mice to construct an in vivo TBI model. Neurological deficits, blood brain barrier (BBB) permeability and brain edema were detected at days 1, 3, and 7 after TBI...
July 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28738820/omega-3-polyunsaturated-fatty-acid-supplementation-attenuates-microglial-induced-inflammation-by-inhibiting-the-hmgb1-tlr4-nf-%C3%AE%C2%BAb-pathway-following-experimental-traumatic-brain-injury
#12
Xiangrong Chen, Shukai Wu, Chunnuan Chen, Baoyuan Xie, Zhongning Fang, Weipeng Hu, Junyan Chen, Huangde Fu, Hefan He
BACKGROUND: Microglial activation and the subsequent inflammatory response in the central nervous system play important roles in secondary damage after traumatic brain injury (TBI). High-mobility group box 1 (HMGB1) protein, an important mediator in late inflammatory responses, interacts with transmembrane receptor for advanced glycation end products (RAGE) and toll-like receptors (TLRs) to activate downstream signaling pathways, such as the nuclear factor (NF)-κB signaling pathway, leading to a cascade amplification of inflammatory responses, which are related to neuronal damage after TBI...
July 24, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28736242/suppression-of-cortical-trpm7-protein-attenuates-oxidative-damage-after-traumatic-brain-injury-via-akt-endothelial-nitric-oxide-synthase-pathway
#13
Hong-Liang Xu, Meng-Dong Liu, Xiao-Hong Yuan, Chun-Xi Liu
Neuronal death after traumatic brain injury (TBI) is a complex process resulting from a combination of factors, many of which are still unknown. Transient receptor potential melastatin 7 (TRPM7) is a transient receptor potential channel that has been demonstrated to mediate ischemic and traumatic neuronal injury in vitro. In the present study, TRPM7 was suppressed in the rat cerebral cortex by intracortical injections of viral vectors bearing shRNA specific for TRPM7 to investigate its potential role in an in vivo TBI model...
July 20, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28713327/il-2-anti-il-2-complex-attenuates-inflammation-and-bbb-disruption-in-mice-subjected-to-traumatic-brain-injury
#14
Weiwei Gao, Fei Li, Ziwei Zhou, Xin Xu, Yingang Wu, Shuai Zhou, Dongpei Yin, Dongdong Sun, Jianhua Xiong, Rongcai Jiang, Jianning Zhang
Traumatic brain injury (TBI) induces the excessive inflammation and disruption of blood-brain barrier, both of which are partially mediated by the activation of microglia and release of inflammatory cytokines. Previous reports showed that administration of regulatory T cells (Tregs) could suppress inflammation and promote neurological function recovery, and that the IL-2/anti-IL-2 complex (IL-2C) could increase the number of Tregs. Thus, we hypothesized that IL-2C-mediated expansion of Tregs would be beneficial in mice subjected to TBI...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28712906/a-comparison-of-pharmacologic-therapeutic-agents-used-for-the-reduction-of-intracranial-pressure-following-traumatic-brain-injury
#15
REVIEW
Ahmed M Alnemari, Brianna M Krafcik, Tarek R Mansour, Daniel Gaudin
OBJECTIVE: In neurotrauma care, a better understanding of treatments following traumatic brain injury (TBI) has led to a significant decrease in morbidity and mortality in this population. TBI represents a significant medical problem, and complications following TBI are associated with the initial injury and post-event intracranial processes such as elevated intracranial pressure (ICP) and brain edema. Consequently, appropriate therapeutic interventions are required to reduce brain tissue damage and improve cerebral perfusion...
July 13, 2017: World Neurosurgery
https://www.readbyqxmd.com/read/28701994/the-role-of-substance-p-in-secondary-pathophysiology-after-traumatic-brain-injury
#16
REVIEW
Robert Vink, Levon Gabrielian, Emma Thornton
It has recently been shown that substance P (SP) plays a major role in the secondary injury process following traumatic brain injury (TBI), particularly with respect to neuroinflammation, increased blood-brain barrier (BBB) permeability, and edema formation. Edema formation is associated with the development of increased intracranial pressure (ICP) that has been widely associated with increased mortality and morbidity after neurotrauma. However, a pharmacological intervention to specifically reduce ICP is yet to be developed, with current interventions limited to osmotic therapy rather than addressing the cause of increased ICP...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28684970/the-effects-of-chunghyul-dan-an-agent-of-korean-medicine-on-a-mouse-model-of-traumatic-brain-injury
#17
Won-Woo Choi, Kyungjin Lee, Beom-Joon Lee, Seong-Uk Park, Jung-Mi Park, Chang-Nam Ko, Youngmin Bu
Chunghyul-Dan (CHD) is the first choice agent for the prevention and treatment of stroke at the Kyung Hee Medical Hospital. To date, CHD has been reported to have beneficial effects on brain disease in animals and humans, along with antioxidative and anti-inflammatory effects. The aim of this study was to evaluate the pharmacological effects of CHD on a traumatic brain injury (TBI) mouse model to explore the possibility of CHD use in patients with TBI. The TBI mouse model was induced using the controlled cortical impact method...
2017: Evidence-based Complementary and Alternative Medicine: ECAM
https://www.readbyqxmd.com/read/28681915/17%C3%AE-estradiol-rescues-damages-following-traumatic-brain-injury-from-molecule-to-behavior-in-mice
#18
Huaihai Lu, Kun Ma, Liwei Jin, He Zhu, Ruiqi Cao
Traumatic brain injury (TBI) is a public health concern, and causes cognitive dysfunction, emotional disorders, and neurodegeration, as well. The currently available treatments are all symptom-oriented with unsatifying efficacy. It is highly demanded to understand its underlying mechanisms. Controlled cortical impact (CCI) was used to induce TBI in aged female mice subjected to ovariectomy. Brain damages were assessed with neurological severity score, brain infarction and edema. Morris water maze and elevated plus maze were applied to evaluate the levels of anxiety...
July 6, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28642177/protective-functions-of-pj34-a-parp-inhibitor-is-related-to-down-regulation-of-calpain-and-nf-%C3%AE%C2%BAb-in-a-mouse-model-of-tbi
#19
Xiaogang Tao, Xuetao Chen, Zonggang Hou, Shuyu Hao, Baiyun Liu
OBJECTIVES: Poly(ADP-ribose) polymerase (PARP), calpain, and nuclear factor-κB (NF-κB) are reported to participate in inflammatory reactions in pathological conditions and are involved in traumatic brain injury. The objective of this study was to investigate whether PARP participated in inflammation related to calpain and NF-κB in a mouse model of controlled cortical impact (CCI). METHODS: PJ34 (10 mg/kg), a selective PARP inhibitor, was administered intraperitoneally 5 min and 8 h after experimental CCI...
June 19, 2017: World Neurosurgery
https://www.readbyqxmd.com/read/28629741/establishment-of-an-ideal-time-window-model-in-hypothermic-targeted-temperature-management-after-traumatic-brain-injury-in-rats
#20
Wan-Yong Zhao, Shao-Bo Chen, Jing-Jing Wang, Chao Xu, Ming-Liang Zhao, Hua-Jiang Dong, Hai-Qian Liang, Xiao-Hong Li, Yue Tu, Sai Zhang, Chong Chen, Hong-Tao Sun
Although hypothermic-targeted temperature management (HTTM) holds great potential for the treatment of traumatic brain injury (TBI), translation of the efficacy of hypothermia from animal models to TBI patientshas no entire consistency. This study aimed to find an ideal time window model in experimental rats which was more in accordance with clinical practice through the delayed HTTM intervention. Sprague-Dawley rats were subjected to unilateral cortical contusion injury and received therapeutic hypothermia at 15 mins, 2 hours, 4 hours respectively after TBI...
June 16, 2017: Brain Research
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