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Stroke reperfusion injury

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https://www.readbyqxmd.com/read/28925323/recanalization-reperfusion-and-recirculation-in-stroke
#1
John H Zhang, Andre Obenaus, David S Liebeskind, Jiping Tang, Richard Hartman, William J Pearce
Recirculation, from arterial inflow routes through venous outflow pathways, was conceptualized in stroke research 50 years ago. As new technologies were developed, blocked arteries could be reopened, capillaries could be reperfused, and the use of recanalization and reperfusion grew to dominate therapeutic strategies. These approaches overwhelmingly focused on restoration of arterial and capillary inflow, but not on veins even though venous disorders may initiate or exacerbate brain injury. In this commentary, we advance the term "recirculation" after "recanalization" and "reperfusion" as a primary concept of stroke pathophysiology that targets the restoration of both the arterial and venous cerebral circulations...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28914132/reverse-electron-transfer-results-in-a-loss-of-flavin-from-mitochondrial-complex-i-potential-mechanism-for-brain-ischemia-reperfusion-injury
#2
Anna Stepanova, Anja Kahl, Csaba Konrad, Vadim Ten, Anatoly S Starkov, Alexander Galkin
Ischemic stroke is one of the most prevalent sources of disability in the world. The major brain tissue damage takes place upon the reperfusion of ischemic tissue. Energy failure due to alterations in mitochondrial metabolism and elevated production of reactive oxygen species (ROS) is one of the main causes of brain ischemia-reperfusion (IR) damage. Ischemia resulted in the accumulation of succinate in tissues, which favors the process of reverse electron transfer (RET) when a fraction of electrons derived from succinate is directed to mitochondrial complex I for the reduction of matrix NAD(+)...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28912645/anti-inflammatory-effect-of-glucagon-like-peptide-1-receptor-agonist-exendin-4-through-modulation-of-ib1-jip1-expression-and-jnk-signaling-in-stroke
#3
Soojin Kim, Jaewon Jeong, Hye-Seon Jung, Bokyung Kim, Ye-Eun Kim, Da-Sol Lim, So-Dam Kim, Yun Seon Song
Glucagon like peptide-1 (GLP-1) stimulates glucose-dependent insulin secretion. Dipeptidyl peptidase-4 (DPP-4) inhibitors, which block inactivation of GLP-1, are currently in clinical use for type 2 diabetes mellitus. Recently, GLP-1 has also been reported to have neuroprotective effects in cases of cerebral ischemia. We therefore investigated the neuroprotective effects of GLP-1 receptor (GLP-1R) agonist, exendin-4 (ex-4), after cerebral ischemia-reperfusion injury. Transient middle cerebral artery occlusion (tMCAO) was induced in rats by intracerebroventricular (i...
August 2017: Experimental Neurobiology
https://www.readbyqxmd.com/read/28887094/salvianolic-acids-for-injection-safi-promotes-functional-recovery-and-neurogenesis-via-sonic-hedgehog-pathway-after-stroke-in-mice
#4
Ye Zhang, Xiangjian Zhang, Lili Cui, Rong Chen, Cong Zhang, Yaoru Li, Tingting He, Xingyuan Zhu, Zuyuan Shen, Lipeng Dong, Jingru Zhao, Ya Wen, Xiufen Zheng, Pan Li
There is a pressing need of developing approaches for delayed post-stroke therapy for patients who fail to receive thrombolysis within the narrow time window. Neuroprotection of Salvianolic Acids for Injection (SAFI) for cerebral ischemia-reperfusion injury in acute phase has been well documented. The current study was to determine the influence of SAFI at the subacute phase after stroke in mice, and to elucidate the underlying mechanisms. Adult male C57BL/6 mice were subjected to permanent occlusion of the distal middle cerebral artery (dMCAO), followed by daily intraperitoneal injection of SAFI 24 h after stroke for 14 days...
September 5, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28886009/tau-mediated-iron-export-prevents-ferroptotic-damage-after-ischemic-stroke
#5
Q-Z Tuo, P Lei, K A Jackman, X-L Li, H Xiong, X-L Li, Z-Y Liuyang, L Roisman, S-T Zhang, S Ayton, Q Wang, P J Crouch, K Ganio, X-C Wang, L Pei, P A Adlard, Y-M Lu, R Cappai, J-Z Wang, R Liu, A I Bush
Functional failure of tau contributes to age-dependent, iron-mediated neurotoxicity, and as iron accumulates in ischemic stroke tissue, we hypothesized that tau failure may exaggerate ischemia-reperfusion-related toxicity. Indeed, unilateral, transient middle cerebral artery occlusion (MCAO) suppressed hemispheric tau and increased iron levels in young (3-month-old) mice and rats. Wild-type mice were protected by iron-targeted interventions: ceruloplasmin and amyloid precursor protein ectodomain, as well as ferroptosis inhibitors...
September 8, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28883427/tau-exacerbates-excitotoxic-brain-damage-in-an-animal-model-of-stroke
#6
Mian Bi, Amadeus Gladbach, Janet van Eersel, Arne Ittner, Magdalena Przybyla, Annika van Hummel, Sook Wern Chua, Julia van der Hoven, Wei S Lee, Julius Müller, Jasneet Parmar, Georg von Jonquieres, Holly Stefen, Ernesto Guccione, Thomas Fath, Gary D Housley, Matthias Klugmann, Yazi D Ke, Lars M Ittner
Neuronal excitotoxicity induced by aberrant excitation of glutamatergic receptors contributes to brain damage in stroke. Here we show that tau-deficient (tau(-/-)) mice are profoundly protected from excitotoxic brain damage and neurological deficits following experimental stroke, using a middle cerebral artery occlusion with reperfusion model. Mechanistically, we show that this protection is due to site-specific inhibition of glutamate-induced and Ras/ERK-mediated toxicity by accumulation of Ras-inhibiting SynGAP1, which resides in a post-synaptic complex with tau...
September 7, 2017: Nature Communications
https://www.readbyqxmd.com/read/28878265/o-glcnacylation-reduces-ischemia-reperfusion-induced-brain-injury
#7
Jin-Hua Gu, Jianhua Shi, Chun-Ling Dai, Jian-Bin Ge, Yang Zhao, Yanxing Chen, Qian Yu, Zheng-Hong Qin, Khalid Iqbal, Fei Liu, Cheng-Xin Gong
O-GlcNAcylation is a common posttranslational modification of nucleocytoplasmic proteins with β-N-acetylglucosamine (GlcNAc) and regulates numerous biological processes. By using mouse models of cerebral ischemia induced by permanent and transient middle cerebral artery occlusion (MCAO), we observed an initial elevation (~1.7-fold, 1-4 hours after ischemia) and then decline of O-GlcNAcylation during cerebral ischemia. We found that moderate increase (<3-fold) of brain O-GlcNAcylation by pharmacological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and neurological deficits...
September 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28874030/synergistic-effects-of-remote-perconditioning-with-terminal-blood-cardioplegia-in-an-in-vivo-piglet-model
#8
Takayuki Abe, Kiyozo Morita, Gen Shinohara, Kazuhiro Hashimoto, Masako Nishikawa
OBJECTIVES: This study tested the hypothesis that remote perconditioning offers effective and synergistic cardioprotection to terminal warm blood cardioplegia for prompt ventricular recovery after prolonged cardioplegic arrest in an in vivo piglet model. METHODS: Twenty-four piglets were subjected to 120 min of single-dose cardioplegic arrest and were divided into 4 groups according to the mode of reperfusion: control (simple aortic unclamp), remote perconditioning, terminal warm blood cardioplegia or remote perconditioning + terminal warm blood cardioplegia; remote perconditioning (4 cycles of 5-min ischaemia-reperfusion of the lower limb) was applied prior to aortic unclamping...
September 1, 2017: European Journal of Cardio-thoracic Surgery
https://www.readbyqxmd.com/read/28870826/hyperforin-protects-against-acute-cerebral-ischemic-injury-through-inhibition-of-interleukin-17a-mediated-microglial-activation
#9
Li Ma, Xia Pan, Fang Zhou, Kang Liu, Long Wang
Hyperforin, a pharmacologically active component of the medicinal plant Hypericum perforatum (St. John's wort), has been shown to be neuroprotective against acute ischemic stroke. However, the underlying mechanisms are still unclear and need to be fully elucidated. C57BL/6 wildtype (WT) mice or interleukin (IL)-17A knock-out mice were subjected to middle cerebral artery occlusion (60 minutes) followed by reperfusion for 72 hours. Hyperforin (0.5 μg) was injected slowly into the right ventricle of WT mice 1, 24 and 48 hours after middle cerebral artery occlusion (MCAO) onset...
September 1, 2017: Brain Research
https://www.readbyqxmd.com/read/28865993/genetic-neutrophil-deficiency-ameliorates-cerebral-ischemia-reperfusion-injury
#10
Ryan A Frieler, Yutein Chung, Carolyn G Ahlers, George Gheordunescu, Jianrui Song, Thomas M Vigil, Yatrik M Shah, Richard M Mortensen
Neutrophils respond rapidly to cerebral ischemia and are thought to contribute to inflammation-mediated injury during stroke. Using myeloid Mcl1 knockout mice as a model of genetic neutrophil deficiency, we investigated the contribution of neutrophils to stroke pathophysiology. Myeloid Mcl1 knockout mice were subjected to transient middle cerebral artery occlusion and infarct size was assessed by MRI after 24h reperfusion. Immune cell mobilization and infiltration was assessed by flow cytometry. We found that myeloid Mcl1 knockout mice had significantly reduced infarct size when compared to heterozygous and wild type control mice (MyMcl1(+/+): 78...
August 31, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28855861/regulation-of-microglia-and-macrophage-polarization-via-apoptosis-signal-regulating-kinase-1-silencing-after-ischemic-hypoxic-injury
#11
So Yeong Cheon, Eun Jung Kim, Jeong Min Kim, Eun Hee Kam, Byung Woong Ko, Bon-Nyeo Koo
Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood-brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inflammatory mediators, which are associated with tissue damage, while those of M2 phenotype release anti-inflammatory mediators, which are related to tissue recovery...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28854438/down-regulation-of-lncrna-malat1-attenuates-neuronal-cell-death-through-suppressing-beclin1-dependent-autophagy-by-regulating-mir-30a-in-cerebral-ischemic-stroke
#12
Dong Guo, Ji Ma, Lei Yan, Tengfei Li, Zhiguo Li, Xinwei Han, Shaofeng Shui
BACKGROUND/AIMS: LncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported to be highly expressed in an in vitro mimic of ischemic stroke conditions. However, the exact biological role of MALAT1 and its underlying mechanism in ischemic stroke remain to be elucidated. METHODS: The roles of MALAT1 and miR-30a on cell death and infarct volume and autophagy were evaluated in experimental ischemic stroke. The relationships between miR-30a and MALAT1, Beclin1 were confirmed by luciferase reporter assay...
August 30, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28851788/regional-transarterial-hypothermic-infusion-in-combination-with-endovascular-thrombectomy-in-acute-ischaemic-stroke-with-cerebral-main-arterial-occlusion-protocol-to-investigate-safety-of-the-clinical-trial
#13
Kikutaro Tokairin, Toshiya Osanai, Takeo Abumiya, Ken Kazumata, Kota Ono, Kiyohiro Houkin
INTRODUCTION: Acute cerebral ischaemia with main cerebral artery occlusion requires treatment with intravenous tissue plasminogen activator administration and/or endovascular thrombectomy. However, some patients fail to recover even after recanalisation because of ischaemia/reperfusion (I/R) injury. We hypothesised that regional transarterial hypothermic infusion would be effective for patients with I/R injury. The aim of this study is to validate the safety of this procedure. METHODS AND ANALYSIS: This is a clinical exploratory study to evaluate safety of regional transarterial hypothermic infusion in combination with endovascular thrombectomy...
August 29, 2017: BMJ Open
https://www.readbyqxmd.com/read/28844957/adiponectin-attenuates-nadph-oxidase-mediated-oxidative-stress-and-neuronal-damage-induced-by-cerebral-ischemia-reperfusion-injury
#14
Xia Li, Hao Guo, Lei Zhao, Bodong Wang, Haixiao Liu, Liang Yue, Hao Bai, Haiyang Jiang, Li Gao, Dayun Feng, Yan Qu
Adiponectin (APN), which is a major adipokine that regulated glucose and lipid metabolism, plays an important role in the protection of the cerebral nervous system. It also has been suggested to have anti-inflammatory effects and ameliorate oxidative stress. Stroke is a universal cause of death and permanent disability. Ischemic stroke accounts for most cases of stroke, and is characterized by cerebral ischemia and neurological deficits. We aimed to investigate the effects of APN-peptide (APN-P) in neurons following ischemia reperfusion (I/R) in C57BL/6J mice, and to study the potential mechanisms underlying its effects...
August 24, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28842824/protein-modifications-with-ubiquitin-as-response-to-cerebral-ischemia-reperfusion-injury
#15
Karin Hochrainer
Post-translational protein modifications present an elegant and energy efficient way to dynamically reprogram cellular protein properties and functions in response to homeostatic imbalance. One such protein modification is the tagging of proteins with the small modifier ubiquitin that can have an impact on protein stability, localization, interaction dynamics, and function. Ubiquitination is vital to any eukaryotic cell under physiological conditions, but even more important under stress including oxidative, genotoxic, and heat stress, where ubiquitination levels are drastically increased...
August 25, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28840056/effects-of-erythropoietin-on-gliogenesis-during-cerebral-ischemic-reperfusion-recovery-in-adult-mice
#16
Rongliang Wang, Jincheng Li, Yunxia Duan, Zhen Tao, Haiping Zhao, Yumin Luo
Erythropoietin (EPO) promotes oligodendrogenesis and attenuates white matter injury in neonatal rats. However, it is unknown whether this effect extends to adult mice and whether EPO regulate microglia polarization after ischemic stroke. Male adult C57BL/6 mice (25-30g) were subjected to 45 min of middle cerebral artery occlusion (MCAO). EPO (5000 IU/kg) or saline was injected intraperitoneally every other day after reperfusion. Neurological function was evaluated using the rotarod test at 1, 3, 7 and 14 days after MCAO...
July 2017: Aging and Disease
https://www.readbyqxmd.com/read/28835447/combining-remote-ischemic-preconditioning-and-aerobic-exercise-a-novel-adaptation-of-blood-flow-restriction-exercise
#17
Justin Daniel Sprick, Caroline A Rickards
Remote ischemic preconditioning (RIPC) can attenuate tissue damage sustained by ischemia-reperfusion injury. Blood flow restriction exercise (BFRE) restricts blood flow to exercising muscles. We implemented a novel approach to BFRE with cyclical bouts of blood flow restriction-reperfusion, reflecting the RIPC model. A concern about BFRE, however, is potential amplification of the exercise pressor reflex, which could be unsafe in at-risk populations. We hypothesized that cyclical BFRE would elicit greater increases in sympathetic outflow and arterial pressure than conventional exercise (CE), performed at the same relative intensity...
August 23, 2017: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28826602/excitatory-and-inhibitory-amino-acid-neurotransmitters-in-stroke-from-neurotoxicity-to-ischemic-tolerance
#18
REVIEW
Diana Amantea, Giacinto Bagetta
The search for neuroprotection in acute ischemic stroke has been dramatically disappointing, with virtually all clinical trials failed for excessive toxicity or lack of efficacy of the tested drug; whereby, current treatments are exclusively based on reperfusion. Given the crucial role of amino acid neurotransmission in ischemic pathobiology, numerous failed strategies were aimed at blocking ionotropic glutamate receptor-mediated excitotoxicity or potentiating GABA-mediated inhibition. Recent work has revived the interest of pharmacologists toward glutamate and GABA receptors, due to a better understanding of subtype-specific toxicity and their involvement in ischemic tolerance...
August 17, 2017: Current Opinion in Pharmacology
https://www.readbyqxmd.com/read/28821706/apigenin-ameliorates-post-stroke-cognitive-deficits-in-rats-through-histone-acetylation-mediated-neurochemical-alterations
#19
Fengxia Tu, Qiongyi Pang, Tingting Huang, Yun Zhao, Meixia Liu, Xiang Chen
BACKGROUND To identify the effect of apigenin on cognitive deficits of rats after cerebral ischemia and reperfusion injury, and to investigate the potential molecular mechanisms. MATERIAL AND METHODS The rats were given sodium butyrate (NaB) or apigenin (20 or 40 mg/kg) for 28 days. Cognition was investigated by the Morris water maze (MWM) test. On day 28, the rats were euthanized and their hippocampal brain regions were used to identify biochemical and neurochemical alterations. The content of histone deacetylase (HDAC) was measured by enzyme-linked immunosorbent assay (ELISA)...
August 19, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28820284/bnip3l-nix-mediated-mitophagy-protects-against-ischemic-brain-injury-independent-of-park2
#20
Yang Yuan, Yanrong Zheng, Xiangnan Zhang, Ying Chen, Xiaoli Wu, Jiaying Wu, Zhe Shen, Lei Jiang, Lu Wang, Wei Yang, Jianhong Luo, Zhenghong Qin, Weiwei Hu, Zhong Chen
Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy. Bnip3l knockout (bnip3l(-/-)) impaired mitophagy and aggravated cerebral I-R injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in park2(-/-) mice, which showed mitophagy deficiency after I-R...
August 18, 2017: Autophagy
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