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https://www.readbyqxmd.com/read/29337840/targeted-temperature-management-at-33%C3%A2-c-or-36%C3%A2-c-produces-equivalent-neuroprotective-effects-in-the-middle-cerebral-artery-occlusion-rat-model-of-ischemic-stroke
#1
Jung Ho Lee, Jisoo Lim, Yong Eun Chung, Sung Phil Chung, Incheol Park, Chul Hoon Kim, Je Sung You
Targeted temperature management (TTM, 32°C to 36°C) is one of the most successful achievements in modern resuscitation medicine. It has become standard treatment for survivors of sudden cardiac arrest to minimize secondary brain damage. TTM at 36°C is just as effective as TTM at 33°C and is actually preferred because it reduces adverse TTM-associated effects. TTM also likely has direct neuroprotective effects in ischemic brains in danger of stroke. It remains unclear, however, whether higher temperature TTM is equally effective in protecting the brain from the effects of stroke...
January 15, 2018: Shock
https://www.readbyqxmd.com/read/29330155/amlexanox-inhibits-cerebral-ischemia-induced-delayed-astrocytic-high-mobility-group-box-1-release-and-subsequent-brain-damage
#2
Sebok Kumar Halder, Hiroshi Ueda
High-mobility group box 1 (HMGB1) is increased in the cerebrospinal fluid (CSF) and serum during the early- and late-phases of brain ischemia and is known to contribute to brain damage. However, detailed characterization underlying cell type-specific HMGB1 release and pathophysiological roles of extracellularly released HMGB1 in ischemic brain remain unclear. Here, we examined cell type-specific HMGB1 release and therapeutic potential of amlexanox, an inhibitor of non-classical release, and an anti-HMGB1 antibody against ischemic brain damage...
January 12, 2018: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/29321396/-molecular-and-cellular-mechanisms-underlying-the-sterile-inflammation-after-ischemic-stroke
#3
Takashi Shichita
Inflammation is an essential step for the pathology of ischemic stroke, and is also an important therapeutic target for developing novel therapeutic methods which have a wide therapeutic time window. Since there is no pathogen in the brain, the inflammation will be triggered by some endogenous molecules which are called as danger associated molecular patterns (DAMPs). So far two important DAMPs, high mobility group box 1 (HMGB1) and peroxiredoxin (PRX), have been recently identified in the ischemic brain. HMGB1 exaggerates the disruption of blood brain barrier; on the other hand, PRX activates mononuclear phagocytes and induces the inflammatory cytokine production through the activation of Toll-like receptor 2 (TLR2) and TLR4...
2018: Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
https://www.readbyqxmd.com/read/29247482/commonalities-in-epileptogenic-processes-from-different-acute-brain-insults-do-they-translate
#4
REVIEW
Pavel Klein, Raymond Dingledine, Eleonora Aronica, Christophe Bernard, Ingmar Blümcke, Detlev Boison, Martin J Brodie, Amy R Brooks-Kayal, Jerome Engel, Patrick A Forcelli, Lawrence J Hirsch, Rafal M Kaminski, Henrik Klitgaard, Katja Kobow, Daniel H Lowenstein, Phillip L Pearl, Asla Pitkänen, Noora Puhakka, Michael A Rogawski, Dieter Schmidt, Matti Sillanpää, Robert S Sloviter, Christian Steinhäuser, Annamaria Vezzani, Matthew C Walker, Wolfgang Löscher
The most common forms of acquired epilepsies arise following acute brain insults such as traumatic brain injury, stroke, or central nervous system infections. Treatment is effective for only 60%-70% of patients and remains symptomatic despite decades of effort to develop epilepsy prevention therapies. Recent preclinical efforts are focused on likely primary drivers of epileptogenesis, namely inflammation, neuron loss, plasticity, and circuit reorganization. This review suggests a path to identify neuronal and molecular targets for clinical testing of specific hypotheses about epileptogenesis and its prevention or modification...
December 15, 2017: Epilepsia
https://www.readbyqxmd.com/read/29245967/genetic-predisposition-to-ischaemic-stroke-by-rage-and-hmgb1-gene-variants-in-chinese-han-population
#5
You Li, Jing Zhu, Linfa Chen, Weidong Hu, Mengxu Wang, Shengnan Li, Xuefeng Gu, Hua Tao, Bin Zhao, Guoda Ma, Keshen Li
Emerging evidence suggests that the multiligand receptor for advanced glycation end products (RAGE) and its ligand high mobility group box 1 protein (HMGB1) contribute to the pathophysiology of ischaemic stroke (IS). The present study aimed to investigate the association of RAGE and HMGB1 variants with the risk of IS. A total of 1,034 patients and 1,015 age- and sex-matched healthy controls were genotyped to detect five genetic variants of the RAGE gene and four genetic variants of the HMGB1 gene using the Multiplex SNaPshot assay...
November 21, 2017: Oncotarget
https://www.readbyqxmd.com/read/29123466/neuroprotective-effect-of-%C3%AE-caryophyllene-on-cerebral-ischemia-reperfusion-injury-via-regulation-of-necroptotic-neuronal-death-and-inflammation-in-vivo-and-in-vitro
#6
Mei Yang, Yongjiu Lv, Xiaocui Tian, Jie Lou, Ruidi An, Qian Zhang, Minghang Li, Lu Xu, Zhi Dong
Necrotic cell death is a hallmark feature of ischemic stroke and it may facilitate inflammation by releasing intracellular components after cell-membrane rupture. Previous studies reported that β-caryophyllene (BCP) mitigates cerebral ischemia-reperfusion (I/R) injury, but the underlying mechanism remains unclear. We explored whether BCP exerts a neuroprotective effect in cerebral I/R injury through inhibiting necroptotic cell death and inflammation. Primary neurons with and without BCP (0.2, 1, 5, 25 μM) treatment were exposed to oxygen-glucose deprivation and re-oxygenation (OGD/R)...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29054968/pivotal-neuroinflammatory-and-therapeutic-role-of-high-mobility-group-box-1-in-ischemic-stroke
#7
Seidu A Richard, Marian Sackey, Zhaoliang Su, Huaxi Xu
Stroke is a major cause of mortality and disability worldwide. Stroke is a frequent and severe neurovascular disorder. The main cause of stroke is atherosclerosis, and the most common risk factor for atherosclerosis is hypertension. Therefore, prevention and treatment of stroke are crucial issues in humans. High mobility group box 1 (HMGB1) is non-histone nuclear protein that is currently one of the crucial pro-inflammatory alarmin in ischemic stroke (IS). It is instantly released from necrotic cells in the ischemic core and activates an early inflammatory response...
October 20, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28912641/toll-like-receptor-2-a-novel-therapeutic-target-for-ischemic-white-matter-injury-and-oligodendrocyte-death
#8
REVIEW
Jun Young Choi, Byung Gon Kim
Despite paramount clinical significance of white matter stroke, there is a paucity of researches on the pathomechanism of ischemic white matter damage and accompanying oligodendrocyte (OL) death. Therefore, a large gap exists between clinical needs and laboratory researches in this disease entity. Recent works have started to elucidate cellular and molecular basis of white matter injury under ischemic stress. In this paper, we briefly introduce white matter stroke from a clinical point of view and review pathophysiology of ischemic white matter injury characterized by OL death and demyelination...
August 2017: Experimental Neurobiology
https://www.readbyqxmd.com/read/28845299/enriched-housing-promotes-post-stroke-functional-recovery-through-astrocytic-hmgb1-il-6-mediated-angiogenesis
#9
Jia-Yi Chen, Yuan Yu, Yin Yuan, Yu-Jing Zhang, Xue-Peng Fan, Shi-Ying Yuan, Jian-Cheng Zhang, Shang-Long Yao
Enriched environment (EE) is shown to promote angiogenesis, neurogenesis and functional recovery after ischemic stroke. However, the underlying mechanisms remain unclear. C57BL/6 mice underwent middle cerebral artery occlusion (60 min) followed by reperfusion, after which mice were housed in either standard environment (SE) or EE. Here we found that post-ischemic EE exhibited decreased depression and anxiety-like behavior, and promoted angiogenesis and functional recovery compared to SE mice. EE mice treated with high-mobility group box-1 (HMGB1) inhibitor glycyrrhizin had an increased post-stroke depression and anxiety-like behavior, and the angiogenesis and functional recovery were decreased...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28732809/oleacein-may-inhibit-destabilization-of-carotid-plaques-from-hypertensive-patients-impact-on-high-mobility-group-protein-1
#10
Agnieszka Filipek, Monika E Czerwińska, Anna K Kiss, Jerzy A Polański, Marek Naruszewicz
BACKGROUND: In patients with hypertension the haemorrhage into carotid atherosclerotic plaque increases risk of plaque destabilization and rupture. Our previous study showed that oleacein, a secoiridoid present in extra virgin olive oil, enhanced uptake of haemoglobin-haptoglobin complex and change macrophage phenotype from pro-inflammatory M1 to anti-inflammatory M2. PURPOSE: The aim this study was to investigate a potential role of oleacein in attenuation of carotid plaque destabilisation ex vivo...
August 15, 2017: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/28645523/elevated-serum-high-mobility-group-box-1-protein-level-is-associated-with-poor-functional-outcome-in-ischemic-stroke
#11
Toshiyuki Tsukagawa, Ryu Katsumata, Mitsugu Fujita, Keizo Yasui, Cassim Akhoon, Kenjiro Ono, Kenji Dohi, Toru Aruga
BACKGROUND: In experimental models, inhibition of high-mobility group box-1 (HMGB1) signaling has been reported to protect against the sequelae of ischemic stroke. Here, we determined the clinical significance of serum HMGB1 levels in patients with acute ischemic stroke. METHODS: We enrolled 183 patients (114 men, 69 women; mean age: 72.7 years) over 6 consecutive months. On admission and day 7, we recorded the National Institutes of Health Stroke Scale scores and measured serum high-sensitivity C-reactive protein (hs-CRP) and HMGB1 levels...
October 2017: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
https://www.readbyqxmd.com/read/28606778/hmgb1-promotes-neurovascular-remodeling-via-rage-in-the-late-phase-of-subarachnoid-hemorrhage
#12
Xiaodi Tian, Liang Sun, Dongxia Feng, Qing Sun, Yang Dou, Chenglin Liu, Feng Zhou, Haiying Li, Haitao Shen, Zhong Wang, Gang Chen
High-mobility group box1 (HMGB1) is a nuclear protein widely expressed in the central nervous system. Extracellular HMGB1 serves as a proinflammatory cytokine and contributes to brain injury during the acute stage post-stroke. Recently, increasing evidence has demonstrated beneficial effects of HMGB1 in some types of brain injury, but little is known about its effects during the late phase of subarachnoid hemorrhage (SAH). This study was designed to explore the potential roles and mechanisms of HMGB1 and its receptor, receptor for advanced glycation end-products (Rage), on brain recovery in the late stage of experimental SAH...
June 9, 2017: Brain Research
https://www.readbyqxmd.com/read/28584116/high-mobility-group-box-1-as-an-autocrine-trophic-factor-in-white-matter-stroke
#13
Jun Young Choi, Yuexian Cui, Samma Tasneem Chowdhury, Byung Gon Kim
Maintenance of white matter integrity in health and disease is critical for a variety of neural functions. Ischemic stroke in the white matter frequently results in degeneration of oligodendrocytes (OLs) and myelin. Previously, we found that toll-like receptor 2 (TLR2) expressed in OLs provides cell-autonomous protective effects on ischemic OL death and demyelination in white matter stroke. Here, we identified high-mobility group box-1 (HMGB1) as an endogenous TLR2 ligand that promotes survival of OLs under ischemic stress...
June 20, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28394332/mafb-prevents-excess-inflammation-after-ischemic-stroke-by-accelerating-clearance-of-damage-signals-through-msr1
#14
Takashi Shichita, Minako Ito, Rimpei Morita, Kyoko Komai, Yoshiko Noguchi, Hiroaki Ooboshi, Ryusuke Koshida, Satoru Takahashi, Tatsuhiko Kodama, Akihiko Yoshimura
Damage-associated molecular patterns (DAMPs) trigger sterile inflammation after tissue injury, but the mechanisms underlying the resolution of inflammation remain unclear. In this study, we demonstrate that common DAMPs, such as high-mobility-group box 1 (HMGB1), peroxiredoxins (PRXs), and S100A8 and S100A9, were internalized through the class A scavenger receptors MSR1 and MARCO in vitro. In ischemic murine brain, DAMP internalization was largely mediated by MSR1. An elevation of MSR1 levels in infiltrating myeloid cells observed 3 d after experimental stroke was dependent on the transcription factor Mafb...
June 2017: Nature Medicine
https://www.readbyqxmd.com/read/28393932/anti-high-mobility-group-box-1-hmgb1-antibody-inhibits-hemorrhage-induced-brain-injury-and-improved-neurological-deficits-in-rats
#15
Dengli Wang, Keyue Liu, Hidenori Wake, Kiyoshi Teshigawara, Shuji Mori, Masahiro Nishibori
As one of the most lethal stroke subtypes, intracerebral hemorrhage (ICH) is acknowledged as a serious clinical problem lacking effective treatment. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. High mobility group box-1 (HMGB1) is a ubiquitous and abundant nonhistone DNA-binding protein, and is also an important proinflammatory molecule once released into the extracellular space from the nuclei...
April 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28152042/effect-of-pregabalin-administration-upon-reperfusion-in-a-rat-model-of-hyperglycemic-stroke-mechanistic-insights-associated-with-high-mobility-group-box-1
#16
Young Song, Ji-Hae Jun, Eun-Jung Shin, Young-Lan Kwak, Jeon-Soo Shin, Jae-Kwang Shim
Hyperglycemia, which reduces the efficacy of treatments and worsens clinical outcomes, is common in stroke. Ability of pregabalin to reduce neuroexcitotoxicity may provide protection against stroke, even under hyperglycemia. We investigated its protective effect against hyperglycemic stroke and its possible molecular mechanisms. Male Wistar rats administered dextrose to cause hyperglycemia, underwent middle cerebral artery occlusion for 1 h and subsequent reperfusion. Rats were treated with an intraperitoneal injection of 30 mg/kg pregabalin or an equal amount of normal saline at the onset of reperfusion (n = 16 per group)...
2017: PloS One
https://www.readbyqxmd.com/read/27784773/leukocyte-response-is-regulated-by-microrna-let7i-in-patients-with-acute-ischemic-stroke
#17
Glen C Jickling, Bradley P Ander, Natasha Shroff, Miles Orantia, Boryana Stamova, Cheryl Dykstra-Aiello, Heather Hull, Xinhua Zhan, DaZhi Liu, Frank R Sharp
OBJECTIVE: To evaluate microRNA let7i in ischemic stroke and its regulation of leukocytes. METHODS: A total of 212 patients were studied: 106 with acute ischemic stroke and 106 controls matched for risk factors. RNA from circulating leukocytes was isolated from blood collected in PAXgene tubes. Let7i microRNA expression was assessed using TaqMan quantitative reverse transcription PCR. To assess let7i regulation of gene expression in stroke, messenger RNA (mRNA) from leukocytes was measured by whole-genome Human Transcriptome Array Affymetrix microarray...
November 22, 2016: Neurology
https://www.readbyqxmd.com/read/27609334/glycyrrhizin-protects-against-focal-cerebral-ischemia-via-inhibition-of-t-cell-activity-and-hmgb1-mediated-mechanisms
#18
Xiaoxing Xiong, Lijuan Gu, Yan Wang, Ying Luo, Hongfei Zhang, Jessica Lee, Sheri Krams, Shengmei Zhu, Heng Zhao
BACKGROUND: Glycyrrhizin (Gly) protects against brain injury induced by stroke. We studied whether Gly achieves its protection by inhibiting T cell activity and high-mobility group box 1 (HMGB1) release in the ischemic brain. METHODS: Stroke was induced by transient middle cerebral artery occlusion in rats and mice. Gly was injected intraperitoneally before or after stroke. We measured infarction, neuroinflammatory cells, gene expressions of interferon-γ (IFNγ), IL-4, and IL-10 in CD4 T cells, HMGB1 release, and T cell proliferation in cultured splenocytes...
September 8, 2016: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/27596007/inhibiting-hmgb1-reduces-cerebral-ischemia-reperfusion-injury-in-diabetic-mice
#19
Chong Wang, Jie Jiang, Xiuping Zhang, Linjie Song, Kai Sun, Ruxiang Xu
High mobility group box1 (HMGB1) promotes inflammatory injury, and accumulating evidence suggests that it plays a key role in brain ischemia reperfusion (I/R), as well as the development of diabetes mellitus (DM). The purpose of this study was to investigate whether HMGB1 plays a role in brain I/R in a DM mouse model. Diabetes mellitus was induced by a high-calorie diet and streptozotocin treatment, and cerebral ischemia was induced by middle cerebral artery occlusion. We examined HMGB1 levels following cerebral I/R injury in DM and non-DM mice and evaluated the influence of altered HMGB1 levels on the severity of cerebral injury...
December 2016: Inflammation
https://www.readbyqxmd.com/read/27544687/hypothermia-inhibits-the-propagation-of-acute-ischemic-injury-by-inhibiting-hmgb1
#20
Jung Ho Lee, Eun Jang Yoon, Jeho Seo, Adriana Kavoussi, Yong Eun Chung, Sung Phil Chung, Incheol Park, Chul Hoon Kim, Je Sung You
Acute ischemic stroke causes significant chronic disability worldwide. We designed this study to clarify the mechanism by which hypothermia helps alleviate acute ischemic stroke. In a middle cerebral artery occlusion model (4 h ischemia without reperfusion), hypothermia effectively reduces mean infarct volume. Hypothermia also prevents neurons in the infarct area from releasing high mobility group box 1 (HMGB1), the most well-studied damage-associated molecular pattern protein. By preventing its release, hypothermia also prevents the typical middle cerebral artery occlusion-induced increase in serum HMGB1...
August 20, 2016: Molecular Brain
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