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ischemic cerebral edema

Yasheng Chen, Rajat Dhar, Laura Heitsch, Andria Ford, Israel Fernandez-Cadenas, Caty Carrera, Joan Montaner, Weili Lin, Dinggang Shen, Hongyu An, Jin-Moo Lee
Although cerebral edema is a major cause of death and deterioration following hemispheric stroke, there remains no validated biomarker that captures the full spectrum of this critical complication. We recently demonstrated that reduction in intracranial cerebrospinal fluid (CSF) volume (∆ CSF) on serial computed tomography (CT) scans provides an accurate measure of cerebral edema severity, which may aid in early triaging of stroke patients for craniectomy. However, application of such a volumetric approach would be too cumbersome to perform manually on serial scans in a real-world setting...
2016: NeuroImage: Clinical
Haiyun Chen, Guolian Tan, Jie Cao, Gaoxiao Zhang, Peng Yi, Pei Yu, Yewei Sun, Zaijun Zhang, Yuqiang Wang
Oxidative stress plays a crucial role in neurological diseases, resulting in excessive production of reactive oxygen species, mitochondrial dysfunction and cell death. In this work, we designed and synthesized a series of tetramethylpyrazine derivatives and investigated their abilities for scavenging free radicals and preventing against oxidative stress-induced neuronal damage in vitro. Among them, compound 22a, consisted of TMP, caffeic acid and a nitrone group, showed potent radical-scavenging activity. Compound 22a had broad neuroprotective effects, including rescuing iodoacetic acid-induced neuronal loss, preventing from t-BHP-induced neuronal injury...
October 14, 2016: Chemical & Pharmaceutical Bulletin
Jing Qiu, Zhongjun Yan, Kai Tao, Yansong Li, Yuqian Li, Jingchen Li, Yushu Dong, Dayun Feng, Huisheng Chen
BACKGROUND: Astrocyte-mediated neuroinflammation plays a critical role in ischemic stroke-induced secondary cerebral injury. Previous studies have suggested that the dopamine D2 receptor (DRD2) acts as a key target in regulating the neuroinflammatory response. However, the underlying molecular mechanisms are still unknown, and effective DRD2 agonists are lacking. In the present study, we examined the anti-inflammatory and neuroprotective effects of sinomenine (Sino), a monomeric compound with potential immunoregulatory properties in nervous system...
October 10, 2016: Journal of Neuroinflammation
Kang-Ho Choi, Hyung-Seok Kim, Man-Seok Park, Eun-Bin Lee, Jung-Kil Lee, Joon-Tae Kim, Ja-Hae Kim, Min-Cheol Lee, Hong-Joon Lee, Ki-Hyun Cho
Cerebral edema from the disruption of the blood-brain barrier (BBB) after cerebral ischemia is a major cause of morbidity and mortality as well as a common event in patients with stroke. Caveolins (Cavs) are thought to regulate BBB functions. Here, we report for the first time that Cav-1 overexpression (OE) decreased brain edema from BBB disruption following ischemic insult. Edema volumes and Cav-1 expression levels were measured following photothrombosis and middle cerebral artery occlusion (MCAO). Endothelial cells that were transduced with a Cav-1 lentiviral expression vector were transplanted into rats...
September 29, 2016: Oncotarget
Chin-Yi Cheng, Yu-Chen Lee
Inflammation plays a crucial role in the pathophysiology of acute ischemic stroke. In the ischemic cascade, resident microglia are rapidly activated in the brain parenchyma and subsequently trigger inflammatory mediator release, which facilitates leukocyte-endothelial cell interactions in inflammation. Activated leukocytes invade the endothelial cell junctions and destroy the blood-brain barrier integrity, leading to brain edema. Toll-like receptors (TLRs) stimulation in microglia/macrophages through the activation of intercellular signaling pathways secretes various proinflammatory cytokines and enzymes and then aggravates cerebral ischemic injury...
2016: Evidence-based Complementary and Alternative Medicine: ECAM
Guanghui Tang, Guo-Yuan Yang
Aquaporin-4 (AQP4) is a family member of water-channel proteins and is dominantly expressed in the foot process of glial cells surrounding capillaries. The predominant expression at the boundaries between cerebral parenchyma and major fluid compartments suggests the function of aquaporin-4 in water transfer into and out of the brain parenchyma. Accumulating evidences have suggested that the dysregulation of aquaporin-4 relates to the brain edema resulting from a variety of neuro-disorders, such as ischemic or hemorrhagic stroke, trauma, etc...
2016: International Journal of Molecular Sciences
Emil Zeynalov, Susan M Jones, J Paul Elliott
Stroke is one of the major causes of morbidity and mortality in the world. Stroke is complicated by brain edema and other pathophysiological events. Among the most important players in the development and evolution of stroke-evoked brain edema is the hormone arginine-vasopressin and its receptors, V1a and V2. Recently, the V1a and V2 receptor blocker conivaptan has been attracting attention as a potential drug to reduce brain edema after stroke. However, animal models which involve conivaptan applications in stroke research need to be modified based on feasible routes of administration...
2016: Journal of Visualized Experiments: JoVE
Alistair J Gunn, Abbot R Laptook, Nicola J Robertson, John D Barks, Marianne Thoresen, Guido Wassink, Laura Bennet
Acute post-asphyxial encephalopathy around the time of birth remains a major cause of death and disability. The possibility that hypothermia may be able to prevent or lessen asphyxial brain injury is a "dream revisited". In this review, a historical perspective is provided from the first reported use of therapeutic hypothermia for brain injuries in antiquity, to the present day. The first uncontrolled trials of cooling for resuscitation were reported more than 50 years ago. The seminal insight that led to the modern revival of studies of neuroprotection was that after profound asphyxia, many brain cells show initial recovery from the insult during a short "latent" phase, typically lasting approximately 6 h, only to die hours to days later after a "secondary" deterioration characterized by seizures, cytotoxic edema, and progressive failure of cerebral oxidative metabolism...
September 27, 2016: Pediatric Research
Kota Kurisu, Takeo Abumiya, Masaki Ito, Masayuki Gekka, Toshiya Osanai, Hideo Shichinohe, Naoki Nakayama, Ken Kazumata, Kiyohiro Houkin
The robust neuroprotective effects of transarterial regional hypothermia have been demonstrated in the typical transient middle cerebral artery occlusion (tMCAO) model, but have not yet been tested in other ischemic stroke models, even though clinical ischemic conditions are diverse. In order to clarify these effects in a different ischemic stroke model, we employed a rat model of permanent MCAO (pMCAO) with transient collateral hypoperfusion (tCHP), which was achieved by direct MCA ligation through craniotomy and 1-hour bilateral common carotid artery occlusion at the beginning of pMCAO...
September 20, 2016: Brain Research
So Y Cheon, Kyoung J Cho, So Y Kim, Eun H Kam, Jong E Lee, Bon-Nyeo Koo
Conditions of increased oxidative stress including cerebral ischemia can lead to blood-brain barrier dysfunction via matrix metalloproteinase (MMP). It is known that MMP-9 in particular is released from brain endothelial cells is involved in the neuronal cell death that occurs after cerebral ischemia. In the intracellular signaling network, apoptosis signal-regulating kinase 1 (ASK1) is the main activator of the oxidative stress that is part of the pathogenesis of cerebral ischemia. ASK1 also promotes apoptotic cell death and brain infarction after ischemia and is associated with vascular permeability and the formation of brain edema...
2016: Frontiers in Cellular Neuroscience
Zhen-Kui Wang, Li Xue, Tao Wang, Xiu-Jie Wang, Zhi-Qiang Su
Invariant natural killer T (iNKT) cells are a unique subset of T cells that have been implicated in inflammation, atopy, autoimmunity, infections, and cancer. Although iNKT cells have been extensively studied over the past decade, its role in the pathogenesis of ischemic brain injury is still largely unknown. In our study, we determined whether iNKT cells infiltration occur in a mouse model of permanent cerebral ischemia. C57BL6/J male mice were treated with either alpha-galactosylceramide (α-GalCer) or vehicle control before undergoing permanent middle cerebral artery occlusion (pMCAO)...
September 13, 2016: Neuroscience Letters
Alireza Partoazar, Sanaz Nasoohi, Sayed Mehdi Rezayat, Kambiz Gilani, Shahram Ejtemaei Mehr, Amir Amani, Nastaran Rahimi, Ahmad Reza Dehpour
Cyclosporin A (CsA) is known as a neuroprotective agent against cerebral ischemia/reperfusion (I/R) in animal models. However, the significant therapeutic effects of CsA have been observed in high systemic doses or manipulating the blood brain barrier (BBB), resulting in systemic side effects and toxicity. Since the liposome nanocarries have been developed for efficient delivery of peptide and proteins, liposomal CsA (Lipo-CsA) could improve cerebral (I/R) injuries. In this study, the liposomal CsA formulation (CsA at dose of 2...
September 12, 2016: Fundamental & Clinical Pharmacology
Yang Yao, Weimin Miao, Zhijia Liu, Wei Han, Kaibin Shi, Yi Shen, Handong Li, Qiang Liu, Ying Fu, DeRen Huang, Fu-Dong Shi
Oxidative stress plays an important role in cerebral ischemia-reperfusion injury. Dimethyl fumarate (DMF) and its primary metabolite monomethyl fumarate (MMF) are antioxidant agents that can activate the nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway and induce the expression of antioxidant proteins. Here, we evaluated the impact of DMF and MMF on ischemia-induced brain injury and whether the Nrf2 pathway mediates the effects provided by DMF and MMF in cerebral ischemia-reperfusion injury...
December 2016: Translational Stroke Research
Juergen Konczalla, Stefan Wanderer, Jan Mrosek, Erdem Gueresir, Patrick Schuss, Johannes Platz, Volker Seifert, Hartmut Vatter
BACKGROUND: Under physiological cerebral conditions, levosimendan, a calcium-channel sensitizer, has a dose-dependent antagonistic effect on prostaglandin F2alpha (PGF)-induced vasoconstriction. This circumstance could be used in antagonizing delayed cerebral vasospasm (dCVS), one of the main complications after subarachnoid hemorrhage (SAH), leading to delayed cerebral ischemia and ischemic neurological deficits. Data already exist that identified neuroprotective effects of levosimendan in a traumatic brain injury model and additionally, it has been proven that this compound prevents narrowing of the basilar artery (BA) luminal area after SAH in an in vitro rabbit model...
November 2016: Acta Neurochirurgica
Courtney J Cook
Induced hypothermia (IH) continues to become a more prevalent treatment modality in neurocritical care. Reducing core temperature has been shown to protect brain tissue during injury and disease. IH has been particularly beneficial in the medical management of refractory intracranial hypertension and malignant cerebral edema. These pathologies are often the result of diffuse cerebral edema after traumatic brain injury, malignant ischemic stroke, or intracerebral hemorrhage. Although there are many benefits to IH, it is not without complications...
September 5, 2016: Journal of Neuroscience Nursing: Journal of the American Association of Neuroscience Nurses
Norio Fujiwara, Angel T Som, Loc-Duyen D Pham, Brian J Lee, Emiri T Mandeville, Eng H Lo, Ken Arai
A free radical scavenger edaravone is clinically used in Japan for acute stroke, and several basic researches have carefully examined the mechanisms of edaravone's protective effects. However, its actions on pro-inflammatory responses under stroke are still understudied. In this study, we subjected adult male Sprague-Dawley rats to 90-min middle cerebral artery (MCA) occlusion followed by reperfusion. Edaravone was treated twice via tail vein; after MCA occlusion and after reperfusion. As expected, edaravone-treated group showed less infarct volume and edema formation compared with control group at 24-h after an ischemic onset...
August 30, 2016: Neuroscience Letters
Guosheng Cao, Nan Jiang, Yang Hu, Yuanyuan Zhang, Guangyun Wang, Mingzhu Yin, Xiaonan Ma, Kecheng Zhou, Jin Qi, Boyang Yu, Junping Kou
Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, has been shown to inhibit cerebral ischemic injury. However, its potential molecular action on blood-brain barrier (BBB) dysfunction after stroke remains unclear. This study aimed to investigate the effects of ruscogenin on BBB dysfunction and the underlying mechanisms in middle cerebral artery occlusion/reperfusion (MCAO/R)-injured mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-injured mouse brain microvascular endothelial cells (bEnd...
2016: International Journal of Molecular Sciences
Mingkun Zhang, Zhenwen Cui, Hua Cui, Yang Cao, Chunlong Zhong, Yong Wang
BACKGROUND: Astaxanthin is a carotenoid pigment that possesses potent antioxidative, anti-inflammatory, antitumor, and immunomodulatory activities. Previous studies have demonstrated that astaxanthin displays potential neuroprotective properties for the treatment of central nervous system diseases, such as ischemic brain injury and subarachnoid hemorrhage. This study explored whether astaxanthin is neuroprotective and ameliorates neurological deficits following traumatic brain injury (TBI)...
2016: BMC Neuroscience
James D Nicholson, Yan Guo, Steven L Bernstein
Ischemia-reperfusion injury after central nervous system (CNS) injury presents a major health care challenge with few promising treatments. Recently, it has become possible to reduce edema after CNS injury by antagonizing a sulfonylurea receptor 1 (SUR1) regulated ion channel expressed after injury. SUR1 upregulation after injury is a necessary precondition for the formation of this channel, and has been implicated in white matter injury after clinical spinal cord trauma. Glibenclamide, an SUR1 antagonist, appears to have neuroprotective effect against cerebral stroke in an open-label small clinical trial and great effectiveness in reducing damage after varied experimental CNS injury models...
2016: PloS One
Alaysia Barrot, Thierry Agm Huisman, Andrea Poretti
Diabetic ketoacidosis (DKA) is a state of severe insulin deficiency and a serious complication in children with diabetes mellitus type 1. In a small number of children, DKA is complicated by injury of the central nervous system. These children have a significant mortality and high long-term neurological morbidity. Cerebral edema is the most common neuroimaging finding in children with DKA and may cause brain herniation. Ischemic or hemorrhagic stroke during the acute DKA episode is less common and accounts for approximately 10% of intracerebral complications of DKA...
October 2016: Neuroradiology Journal
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