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virally TBI rat

Li-Hua Chen, Hong-Tian Zhang, Ru-Xiang Xu, Wen-De Li, Hao Zhao, Yi Yang, Kai Sun
Objectives: methyl-D-aspartate NMDA receptor (NMDAR) and aquaporin 4 (AQP4) are involved in the molecular cascade of edema after traumatic brain injury (TBI) and are potential targets of studies in pharmacology and medicine. However, their association and interactions are still unknown. Materials and Methods: We established a rat TBI model in this study. The cellular distribution patterns of AQP4 after inhibition of NMDAR were determined by Western blotting and immunoreactive staining...
November 2018: Iranian Journal of Basic Medical Sciences
Mattias Günther, Faiez Al Nimer, Fredrik Piehl, Mårten Risling, Tiit Mathiesen
Traumatic brain injury (TBI) leads to a deleterious and multifactorial secondary inflammatory response in the brain. Oxidative stress from the inflammation likely contributes to the brain damage although it is unclear to which extent. A largely unexplored approach is to consider phenotypic regulation of oxidative stress levels. Genetic polymorphism influences inflammation in the central nervous system and it is possible that the antioxidative response differs between phenotypes and affects the severity of the secondary injury...
March 2018: ENeuro
Deborah R Boone, Jeanna M Leek, Michael T Falduto, Karen E O Torres, Stacy L Sell, Margaret A Parsley, Jeremy C Cowart, Tatsuo Uchida, Maria-Adelaide Micci, Douglas S DeWitt, Donald S Prough, Helen L Hellmich
Virally mediated RNA interference (RNAi) to knock down injury-induced genes could improve functional outcome after traumatic brain injury (TBI); however, little is known about the consequences of gene knockdown on downstream cell signaling pathways and how RNAi influences neurodegeneration and behavior. Here, we assessed the effects of adeno-associated virus (AAV) siRNA vectors that target two genes with opposing roles in TBI pathogenesis: the allegedly detrimental neuronal nitric oxide synthase (nNOS) and the potentially protective glutathione peroxidase 1 (GPx-1)...
2017: PloS One
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...
January 2018: Neurochemistry International
Ji Ma, Shaofeng Shui, Xinwei Han, Dong Guo, Tengfei Li, Lei Yan
Traumatic brain injury (TBI) is a major cause of injury-related deaths, and the mechanism of TBI has become a research focus, but little is known about the mechanism of microRNAs in TBI. The aim of this study is the role of microRNA-22 (miR-22) in TBI-induced neuronal cell apoptosis. Rat cortical neurons were cultured and the TBI model was induced by scratch injury in vitro, before which miR-22 level was altered by transfection of agomir or antagomir. Lactate dehydrogenase (LDH) release and TUNEL assays were performed to examine neuronal cell injury and apoptosis...
2016: American Journal of Translational Research
Chi Liu, Ping Zhu, Taro Saito, Yoshitaka Isaka, Yukitoshi Nagahara, Jian Zhuang, Xiao-Kang Li
Organ transplant recipients have elevated cancer and viral infection risks due to immunosuppression and long-term results of organ transplantation remain unsatisfactory, mainly because of chronic rejection. The purpose of the current study is to establish a nonmyeloablative perioperative regimen, able to induce mixed chimerism and tolerance of allografts. To establish a nonmyeloablative perioperative regimen, we used Busulfan, an important component of many bone marrow transplantation preparative regimens for a variety of non-neoplastic diseases as an alternative to total body irradiation (TBI), and FTY720, a unique immunosuppression agent, inhibition lymphocyte homing...
July 2013: International Immunopharmacology
Marek Ma, Frances S Shofer, Robert W Neumar
Traumatic brain injury (TBI) causes substantial morbidity and mortality worldwide. A key component of both mild and severe TBI is diffuse axonal injury. Except in cases of extreme mechanical strain, when axons are torn at the moment of trauma, axonal stretch injury is characterized by early cytoskeletal proteolysis, transport disruption, and secondary axotomy. Calpains, a family of Ca(2+)-dependent proteases, have been implicated in this pathologic cascade, but direct in vivo evidence is lacking. To test the hypothesis that calpains play a causal role in axonal stretch injury in vivo, we used our rat optic nerve stretch model following adeno-associated viral (AAV) vector-mediated overexpression of the endogenous calpain inhibitor calpastatin in optic nerve axons...
November 1, 2012: Journal of Neurotrauma
M L Degeorge, D Marlowe, E Werner, K E Soderstrom, M Stock, A Mueller, M C Bohn, D A Kozlowski
Our laboratory has previously demonstrated that viral administration of glial cell line-derived neurotrophic factor (AdGDNF), one week prior to a controlled cortical impact (CCI) over the forelimb sensorimotor cortex of the rat (FL-SMC) is neuroprotective, but does not significantly enhance recovery of sensorimotor function. One possible explanation for this discrepancy is that although protected, neurons may not have been functional due to enduring metabolic deficiencies. Additionally, metabolic events following TBI may interfere with expression of therapeutic proteins administered to the injured brain via gene therapy...
July 27, 2011: Brain Research
Hongtao Wu, Hao Jiang, Dunyue Lu, Changsheng Qu, Ye Xiong, Dong Zhou, Michael Chopp, Asim Mahmood
BACKGROUND: Our previous studies demonstrated that simvastatin reduced neuronal death, increased neurogenesis, and promoted functional recovery after traumatic brain injury (TBI). OBJECTIVE: To investigate the effect of simvastatin on angiogenesis after TBI and the related signaling pathways. METHODS: Saline or simvastatin (1 mg/kg) was administered orally to rats starting at day 1 after TBI or sham surgery and then daily for 14 days. Rats were sacrificed at 3 and 14 days after treatment...
May 2011: Neurosurgery
Jennie E Minnich, Sarah L Mann, Megan Stock, Kathryn A Stolzenbach, Bridget M Mortell, Katherine E Soderstrom, Martha C Bohn, Dorothy A Kozlowski
PURPOSE: The therapeutic potential of glial cell line-derived neurotrophic factor (GDNF) gene delivery was examined in a rodent model of traumatic brain injury (TBI), the controlled cortical impact (CCI). METHODS: An adenoviral vector harboring human GDNF (AdGDNF) or green fluorescent protein (AdGFP) was injected unilaterally into the forelimb sensorimotor cortex (FL-SMC) of the rat one week prior to a unilateral CCI. Tests of forelimb function and asymmetry were administered for 2 weeks post-injury...
2010: Restorative Neurology and Neuroscience
Hongtao Wu, Dunyue Lu, Hao Jiang, Ye Xiong, Changsheng Qu, Bo Li, Asim Mahmood, Dong Zhou, Michael Chopp
This study was undertaken to evaluate the effect of simvastatin, a cholesterol-lowering agent, on the Akt-mediated signaling pathway and neurogenesis in the dentate gyrus (DG) of the hippocampus in rats after traumatic brain injury (TBI). Adult male Wistar rats were divided into three groups: (1) sham group (n = 8); (2) saline control group (n = 40); and (3) simvastatin-treated group (n = 40). Controlled cortical impact (CCI) injury was performed over the left parietal lobe. Simvastatin was administered orally at a dose of 1 mg/kg starting at day 1 after TBI and then daily for 14 days...
February 2008: Journal of Neurotrauma
Girish J Kotwal, Debomoy K Lahiri, Ramona Hicks
Traumatic brain injury (TBI) is one of the few known risk factors for Alzheimers disease (AD) and for depression. The mechanisms by which trauma causes delayed cognitive deficits are largely unknown. In recent studies, it was demonstrated that the complement system (an important component of the immune system and a mediator of inflammation) is activated both in human AD and following experimental TBI in rats. Amyloid proteins are also present in AD and following TBI, and are known to activate complement in vitro...
November 2002: Annals of the New York Academy of Sciences
Linglong Zou, Patricia Yotnda, Tiejun Zhao, Xiaoqing Yuan, Yan Long, Heshan Zhou, Keyi Yang
Traumatic brain injury (TBI) causes delayed neuronal deficits that in principle could be prevented by timely intervention with therapeutic genes. However, appropriate vectors for gene transfer to the brain with TBI remain to be developed. First-generation adenoviruses (fgAd) are usually associated with inflammatory and toxic effects when inoculated into brains, despite their high efficiency of gene transfer to these tissues. In this study the authors attempted to determine whether a less immunogenic gene-transfer protocol can be established in the traumatically injured rat brain using helper-dependent adenoviruses (hdAd), a novel adenoviral construct with full deletion of viral coding sequences...
August 2002: Journal of Cerebral Blood Flow and Metabolism
Ramona R Hicks, Kristen L Keeling, Ming-Yan Yang, Scott A Smith, Ann M Simons, Girish J Kotwal
Inflammation is a major contributor to the neuropathological consequences of traumatic brain injury (TBI). Previous studies have shown that proinflammatory complement activation fragments are present in the injured brain within the first 24 h after trauma. To investigate whether complement activation within the injured brain leads to the neuropathology and subsequent functional impairment associated with TBI, we examined what effect administration of a complement inhibitor, the vaccinia virus complement control protein (VCP), would have on spatial learning and memory in brain injured rats, as measured using the Morris Water Maze (MWM) procedure...
June 2002: Journal of Neurotrauma
F L Li, G Grauls, M Yin, C A Bruggeman
We previously demonstrated that cytomegalovirus (CMV) infection enhanced perivascular inflammation in rat aortic allografts. In this study, we investigated the relationship between the CMV infection load and the magnitude of perivasculitis (chronic rejection) in aortic transplants. Rats received orthotopic abdominal aortic grafts, different degrees of total body irradiation (TBI) for immunosuppression and CMV inoculation. The spleens of the rats receiving 5 Gy of TBI contained more infectious virus and viral antigens than those of rats receiving 3 Gy of TBI or no TBI...
1996: Transplant International
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