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hmgb1 stroke

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
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
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...
2016: Journal of Neuroinflammation
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
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...
2016: Molecular Brain
Xiaodi Tian, Zhong Wang, Gang Chen
High mobility group box-1 (HMGB1), a highly conserved nonhistone nuclear protein, is widely expressed in most eukaryotic cells including neural cells. Nuclear HMGB1 stabilize nucleosome formation and facilitates gene transcription. HMGB1 can be passively released from necrotic cells or actively secreted from stimulated immune cells. Extracellular HMGB1 interacts with receptors, including the receptor for advanced glycation endproducts (RAGEs), Toll-like receptor 2 (TLR2) and TLR4. After brain injury, HMGB1 is released early from neural cells and contribute to the early stages of the inflammatory response...
August 8, 2016: Current Drug Delivery
Shinichi Harada, Wataru Matsuura, Keyue Liu, Masahiro Nishibori, Shogo Tokuyama
Central post-stroke pain (CPSP) is one of the most under-recognized consequences of cerebral stroke, but the development of an effective treatment strategy is urgent. High-mobility group box 1 (HMGB1) and the receptor for advanced glycation end products (RAGE, one of the receptors of HMGB1) have recently been shown to be critical in the modulation of nociceptive transduction following peripheral neuropathy. The aim of this study was to determine the interactions between CPSP and HMGB1/RAGE signaling. Male ddY mice were subjected to 30min of bilateral carotid artery occlusion (BCAO)...
September 1, 2016: Brain Research
Hideo Takahashi, Masahiro Nishibori
High mobility group box protein1 (HMGB1), a ubiquitous chromatin component, is released by necrotic cells, apoptotic cells, and cells in profound distress. HMGB1 plays a critical role as a proinflammatory mediator. HMGB1 represents an important new target for drug development in a variety of inflammatory disorders, including stroke, brain injury, arteriosclerosis, and cancer. The antibodies against HMGB1 and its receptors ar hopeful candidates for immunotherapeutic strategy for treating patients with these diseases...
April 2016: Nihon Rinsho. Japanese Journal of Clinical Medicine
Kazuo Yamagata, Natumi Sone, Sari Suguyama, Toru Nabika
Stroke-prone spontaneously hypertensive rats (SHRSP/Izm) develop severe hypertension and astrocytic oedema following ischaemic stimulation. During ischaemic stress high-mobility group box 1 (Hmgb1) expression in astrocytes is induced, and subsequently potentiates deterioration of the brain due to ischaemic injury, which manifests as both cerebral inflammation and astrocytic oedema. Arginine vasopressin (AVP) induces brain injury and increases astrocytic swelling. After stroke, Hmgb1 and peroxiredoxin (Prx) are released at different times and activate macrophages in the brain via Toll-like receptors (Tlr2s)...
April 2016: International Journal of Experimental Pathology
Leila Sadat-Hatamnezhad, Asghar Tanomand, Javad Mahmoudi, Siamak Sandoghchian Shotorbani
BACKGROUND: Stroke is a leading cause of death all around the world, and ischemic stroke is considered to be the most common stroke type. Toll-like receptors (TLRs) are important molecules for detection of both pathogen invasion and tissue damage. In this regard, the purpose of this study was to assess the expression level of TLR2 on monocytes in patients with ischemic stroke and to evaluate the expression change profile following high-mobility group box 1 (HMGB1) stimulation. METHODS: A total of 30 patients with ischemic stroke were enrolled from November 2013 to September 2014...
September 2016: Iranian Biomedical Journal
J Hu, B Liu, Q Zhao, P Jin, F Hua, Z Zhang, Y Liu, K Zan, G Cui, X Ye
High-mobility group box 1 (HMGB1), a ligand of receptor for advanced glycation endproducts (RAGE), functions as a proinflammatory factor. It is mainly involved in inflammatory activation and contributes to the initiation and progression of stroke. By using a model of transient middle cerebral artery occlusion (MCAo) in type 2 diabetic rats, we investigated the changes of pro-inflammation mediators, blood-brain barrier (BBB) leakage and functional outcome after stroke. Type 2 diabetic rats did not show an increased lesion volume, but exhibited significantly increased expression of HMGB1 and RAGE, BBB leakage, as well as decreased functional outcome after stroke compared with control rats...
June 2, 2016: Neuroscience
Yoshihiko Nakamura, Takafumi Nakano, Keiichi Irie, Kazunori Sano, Junichi Tanaka, Yuta Yamashita, Tomomitsu Satho, Koichi Matsuo, Masayuki Fujioka, Hiroyasu Ishikura, Kenichi Mishima
BACKGROUND: It has been reported that recombinant human soluble thrombomodulin (rhsTM) has a high-mobility group box (HMGB)1 inhibitory effect. Some investigators reported that HMGB1 is associated with ischemic stroke. However, there have been no previous studies to determine whether rhsTM can ameliorate cerebral ischemic injury through its HMGB1 inhibitory mechanism in ischemic stroke. We investigated the effects of rhsTM on cerebral ischemic injury in a 4-h middle cerebral artery occlusion (MCAO) murine model...
March 15, 2016: Journal of the Neurological Sciences
Jue Wang, Dong Han, Miao Sun, Juan Feng
Remote ischemic perconditioning (RIPerC) and ischemic postconditioning (IPOC) are well-acknowledged neuroprotective procedures during ischemic injury. The present study established a combined RIPerC and IPOC (RIPerC + IPOC) model in rats and studied how it would regulate the autophagy process and affect HMGB1 levels in a rat model of middle cerebral artery occlusion (MCAO). Rats with MCAO were treated with RIPerC by fastening and release of the left hind limb to achieve 4 cycles of 5 min remote ischemia reperfusion, 40 min prior to cerebral reperfusion, and then treated with IPOC by exposing the cerebral middle artery to 3 cycles of 30 s reperfusion/30 s occlusion at the onset of cerebral reperfusion...
April 2016: Journal of Molecular Neuroscience: MN
Ilknur Ay, Rena Nasser, Bruce Simon, Hakan Ay
BACKGROUND: Direct stimulation of the vagus nerve in the neck via surgically implanted electrodes is protective in animal models of stroke. We sought to determine the safety and efficacy of a non-invasive cervical VNS (nVNS) method using surface electrodes applied to the skin overlying the vagus nerve in the neck in a model of middle cerebral artery occlusion (MCAO). METHODS: nVNS was initiated variable times after MCAO in rats (n = 33). Control animals received sham stimulation (n = 33)...
March 2016: Brain Stimulation
Vikramjeet Singh, Stefan Roth, Roland Veltkamp, Arthur Liesz
SIGNIFICANCE: Stroke is the leading cause of morbidity and mortality worldwide. Inflammatory cascades have a major impact on outcome and regeneration after ischemic stroke. High-mobility group box 1 (HMGB1) has come into the focus of experimental and clinical stroke research because it is released from necrotic brain tissue and its differential redox forms attract and activate immune cells after ischemic brain injury. HMGB1 is a potent inducer of inflammatory cascades, and thereby, secondary deterioration of neurological outcome...
April 20, 2016: Antioxidants & Redox Signaling
Takafumi Nakano, Keiichi Irie, Kazuhide Hayakawa, Kazunori Sano, Yoshihiko Nakamura, Masayoshi Tanaka, Yuta Yamashita, Tomomitsu Satho, Masayuki Fujioka, Carl Muroi, Koichi Matsuo, Hiroyasu Ishikura, Kojiro Futagami, Kenichi Mishima
Tissue plasminogen activator (tPA) is the only approved therapy for acute ischemic stroke. However, delayed tPA treatment increases the risk of cerebral hemorrhage and can result in exacerbation of nerve injury. ADAMTS13, a von Willebrand factor (VWF) cleaving protease, has a protective effect against ischemic brain injury and may reduce bleeding risk by cleaving VWF. We examined whether ADAMTS13 has a longer therapeutic time window in ischemic stroke than tPA in mice subjected to middle cerebral artery occlusion (MCAO)...
October 22, 2015: Brain Research
Hyong Woo Choi, Miaoying Tian, Fei Song, Emilie Venereau, Alessandro Preti, Sang-Wook Park, Keith Hamilton, G V T Swapna, Murli Manohar, Magali Moreau, Alessandra Agresti, Andrea Gorzanelli, Francesco De Marchis, Huang Wang, Marc Antonyak, Robert J Micikas, Daniel R Gentile, Richard A Cerione, Frank C Schroeder, Gaetano T Montelione, Marco E Bianchi, Daniel F Klessig
Salicylic acid (SA) and its derivatives have been used for millennia to reduce pain, fever and inflammation. In addition, prophylactic use of acetylsalicylic acid, commonly known as aspirin, reduces the risk of heart attack, stroke and certain cancers. Because aspirin is rapidly de-acetylated by esterases in human plasma, much of aspirin's bioactivity can be attributed to its primary metabolite, SA. Here we demonstrate that human high mobility group box 1 (HMGB1) is a novel SA-binding protein. SA-binding sites on HMGB1 were identified in the HMG-box domains by nuclear magnetic resonance (NMR) spectroscopic studies and confirmed by mutational analysis...
2015: Molecular Medicine
Cheng-Yi Chang, Tsung-Kuei Kao, Wen-Ying Chen, Yen-Chuan Ou, Jian-Ri Li, Su-Lan Liao, Shue-Ling Raung, Chun-Jung Chen
Experimental studies have demonstrated the beneficial effects of tetramethylpyrazine (TMP) against ischemic stroke and highlighted its crucial role in anti-inflammatory activity. This study provides evidence of an alternative target for TMP and sheds light on the mechanism of its anti-inflammatory action against ischemic brain injury. We report a global inhibitory effect of TMP on inflammatory cell intracerebral activation and infiltration in a rat model of permanent cerebral ischemia. The results of immunohistochemistry, enzymatic assay, flow cytometric analysis, and cytological analysis revealed that intraperitoneal TMP administration reduced neuronal loss, macrophage/microglia activation, brain parenchyma infiltrative neutrophils, and circulating neutrophils after cerebral ischemia...
July 31, 2015: Biochemical and Biophysical Research Communications
C F Tsao, W T Huang, T T Liu, P W Wang, C W Liou, T K Lin, C J Hsieh, S W Weng
The role of high mobility group box 1 (HMGB1) has been demonstrated in stroke and coronary artery disease but not in peripheral arterial occlusive disease (PAOD). The pathogenesis of HMGB1 in acute and chronic vascular injury is also not well understood. We hypothesized that HMGB1 induces inflammatory markers in diabetic PAOD patients. We studied 36 diabetic patients, including 29 patients with PAOD, who had undergone amputation for diabetic foot and 7 nondiabetic patients who had undergone amputation after traumatic injury...
2015: Genetics and Molecular Research: GMR
Haiyang Fang, Rongcai Yue, Yang Ga, Yi Zhang, Lei Shan, Jing Zhao
Ischemic stroke is the third leading cause of death in the world. Our previous study found that cynandione A (CYNA), the main component from the root of Cynanchum bungei, exhibits anti-ischemic stroke activity. In this work, we investigated the therapeutic mechanisms of CYNA to ischemic stroke at protein network level. First, PC12 cells and cerebellar granule neurons were prepared to validate the effects of CYNA against glutamate injury. Our experiments suggested that CYNA could dose-dependently mitigate glutamate-induced neurons neurotoxicity and inhibit glutamate-induced upregulation of KHSRP and HMGB1, further confirming the neuroprotective effects of CYNA in vivo...
2015: PloS One
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