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Stroke reperfusion injury

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https://www.readbyqxmd.com/read/28645333/sac-1004-a-vascular-leakage-blocker-reduces-cerebral-ischemia-reperfusion-injury-by-suppressing-blood-brain-barrier-disruption-and-inflammation
#1
Haiying Zhang, Joon Ha Park, Sony Maharjan, Jeong Ae Park, Kyu-Sung Choi, Hyojin Park, Yoonjeong Jeong, Ji Hyeon Ahn, In Hye Kim, Jae-Chul Lee, Jeong Hwi Cho, In-Kyu Lee, Choong Hyun Lee, In Koo Hwang, Young-Myeong Kim, Young-Ger Suh, Moo-Ho Won, Young-Guen Kwon
BACKGROUND: Blood-brain barrier (BBB) breakdown and inflammation are critical events in ischemic stroke, contributing to aggravated brain damage. The BBB mainly consists of microvascular endothelial cells sealed by tight junctions to protect the brain from blood-borne substances. Thus, the maintenance of BBB integrity may be a potential target for neuroprotection. Sac-1004, a pseudo-sugar derivative of cholesterol, enhances the endothelial barrier by the stabilization of the cortical actin ring...
June 23, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28641323/ischaemia-reperfusion-injury-and-hyperbaric-oxygen-pathways-a-review-of-cellular-mechanisms
#2
REVIEW
Ashish Francis, Richard Baynosa
Ischaemia-induced tissue injury has wide-ranging clinical implications including myocardial infarction, stroke, compartment syndrome, ischaemic renal failure and replantation and revascularization. However, the restoration of blood flow produces a 'second hit' phenomenon, the effect of which is greater than the initial ischaemic event and characterizes ischaemia-reperfusion (IR) injury. Some examples of potential settings of IR injury include: following thrombolytic therapy for stroke, invasive cardiovascular procedures, solid organ transplantation, and major trauma resuscitation...
June 2017: Diving and Hyperbaric Medicine: the Journal of the South Pacific Underwater Medicine Society
https://www.readbyqxmd.com/read/28638888/modulation-of-key-biochemical-markers-relevant-to-stroke-by-antiaris-africana-leaf-extract-following-cerebral-ischemia-reperfusion-injury
#3
Omotayo B Ilesanmi, Afolabi C Akinmoladun, Olanrewaju Sam Olayeriju, Ibrahim Olabayode Saliu, M Tolulope Olaleye, Afolabi A Akindahunsi
BACKGROUND: Oxidative stress plays a significant role in stroke pathogenesis. Hence, plants rich in antioxidant phytochemicals have been suggested as effective remedies for prevention and treatment of stroke and other neurological diseases. Antiaris africana Engl. (Moraceae) is traditionally used for the management of brain-related problems but there is paucity of data on its anti-stroke potential. MATERIALS AND METHODS: Ischemia/reperfusion injury was induced by a 30 min bilateral common carotid artery occlusion/ 2 h reperfusion (BCCAO/R) in the brain of male Wistar rats...
2017: African Journal of Traditional, Complementary, and Alternative Medicines: AJTCAM
https://www.readbyqxmd.com/read/28634421/the-role-of-von-willebrand-factor-in-vascular-inflammation-from-pathogenesis-to-targeted-therapy
#4
REVIEW
Felice Gragnano, Simona Sperlongano, Enrica Golia, Francesco Natale, Renatomaria Bianchi, Mario Crisci, Fabio Fimiani, Ivana Pariggiano, Vincenzo Diana, Andreina Carbone, Arturo Cesaro, Claudia Concilio, Giuseppe Limongelli, Mariagiovanna Russo, Paolo Calabrò
Beyond its role in hemostasis, von Willebrand factor (VWF) is an emerging mediator of vascular inflammation. Recent studies highlight the involvement of VWF and its regulator, ADAMTS13, in mechanisms that underlie vascular inflammation and immunothrombosis, like leukocyte rolling, adhesion, and extravasation; vascular permeability; ischemia/reperfusion injury; complements activation; and NETosis. The VWF/ADAMTS13 axis is implicated in the pathogenesis of atherosclerosis, promoting plaque formation and inflammation through macrophage and neutrophil recruitment in inflamed lesions...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28634116/succinate-induced-neuronal-mitochondrial-fission-and-hexokinase-ii-malfunction-in-ischemic-stroke-therapeutical-effects-of-kaempferol
#5
Bin Wu, Hong Luo, Xu Zhou, Cai-Yi Cheng, Lin Lin, Bao-Lin Liu, Kang Liu, Ping Li, Hua Yang
Mitochondrial dysfunction is known as one of causative factors in ischemic stroke, leading to neuronal cell death. The present work was undertaken to investigate whether succinate induces neuron apoptosis by regulating mitochondrial morphology and function. In neurons, oxygen-glucose deprivation induced succinate accumulation due to the reversal of succinate dehydrogenase (SDH) activation, leading to mitochondrial fission. Kaempferol inhibited mitochondrial fission and maintained mitochondrial HK-II through activation of Akt, and thereby protected neurons from succinate-mediated ischemi injury...
June 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28629771/chemokines-play-complex-roles-in-cerebral-ischemia
#6
REVIEW
Chen Chen, Shi-Feng Chu, Dan-Dan Liu, Zhao Zhang, Ling-Lei Kong, Xin Zhou, Nai-Hong Chen
Ischemic stroke (IS) is a disease caused by deficiency of blood and oxygen in focal or complete brain, followed by inflammation cascade and other pathological reactions, which finally lead to irreversible damage to the cerebrum. For the inflammation is a key progress at the initiation of ischemia and poststroke, and chemokines work as vital cytokines in inflammation, we focus the roles of chemokines in IS. Studies have shown cerebral ischemia is associated with marked induction of both CXC and CC chemokines which resulting in extensive leukocyte infiltration in the ischemic brain, and neutrophil infiltration may increase cerebral edema inducing injury in the ischemic area...
June 16, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28629519/erythropoietin-endogenous-protection-of-ischemic-brain
#7
Robert T Mallet, Myoung-Gwi Ryou
The human brain requires uninterrupted delivery of blood-borne oxygen and nutrients to sustain its function. Focal ischemia, particularly, ischemic stroke, and global ischemia imposed by cardiac arrest disrupt the brain's fuel supply. The resultant ATP depletion initiates a complex injury cascade encompassing intracellular Ca(2+) overload, glutamate excitotoxicity, oxido-nitrosative stress, extracellular matrix degradation, and inflammation, culminating in neuronal and astroglial necrosis and apoptosis, neurocognitive deficits, and even death...
2017: Vitamins and Hormones
https://www.readbyqxmd.com/read/28626056/early-reperfusion-after-brain-ischemia-has-beneficial-effects-beyond-rescuing-neurons
#8
Masaki Tachibana, Tetsuro Ago, Yoshinobu Wakisaka, Junya Kuroda, Masahiro Shijo, Yoji Yoshikawa, Motohiro Komori, Ataru Nishimura, Noriko Makihara, Kuniyuki Nakamura, Takanari Kitazono
BACKGROUND AND PURPOSE: Recent studies show that successful endovascular thrombectomy 6 to 12 hours after stroke onset enhances functional outcomes 3 months later. In this study, we investigated the effects of reperfusion after ischemia on repair processes in the ischemic areas, as well as on functional recovery, using mouse stroke models. METHODS: We examined time-dependent histological changes and functional recovery after transient middle cerebral artery occlusion of different durations, including permanent middle cerebral artery occlusion, using the CB-17 (CB-17/lcr-+/+Jcl) mouse strain, which has poor pial collateral blood flow...
June 16, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/28624878/a-combination-of-three-repurposed-drugs-administered-at-reperfusion-as-a-promising-therapy-for-postischemic-brain-injury
#9
I-Chen Yu, Ping-Chang Kuo, Jui-Hung Yen, Hallel C Paraiso, Eric T Curfman, Benecia C Hong-Goka, Robert D Sweazey, Fen-Lei Chang
Cerebral ischemia leads to multifaceted injury to the brain. A polytherapeutic drug that can be administered immediately after reperfusion may increase protection to the brain by simultaneously targeting multiple deleterious cascades. This study evaluated efficacy of the combination of three clinically approved drugs: lamotrigine, minocycline, and lovastatin, using two mouse models: global and focal cerebral ischemia induced by transient occlusion of the common carotid arteries or the middle cerebral artery, respectively...
June 17, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28620235/a-non-ionotropic-activity-of-nmda-receptors-contributes-to-glycine-induced-neuroprotection-in-cerebral-ischemia-reperfusion-injury
#10
Juan Chen, Rong Hu, Huabao Liao, Ya Zhang, Ruixue Lei, Zhifeng Zhang, Yang Zhuang, Yu Wan, Ping Jin, Hua Feng, Qi Wan
NMDA receptor (NMDAR) is known for its ionotropic function. But recent evidence suggests that NMDAR also has a non-ionotropic property. To determine the role of non-ionotropic activity of NMDARs in clinical relevant conditions, we tested the effect of glycine, a co-agonist of NMDARs, in rat middle cerebral artery occlusion (MCAO), an animal model of cerebral ischemia-reperfusion injury after the animals were injected with the NMDAR channel blocker MK-801 and the glycine receptor antagonist strychnine. We show that glycine reduces the infarct volume in the brain of ischemic stroke animals pre-injected with MK-801 and strychnine...
June 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28612530/-minocycline-prevent-microglial-activation-via-suppression-of-adenosine-a-2a-receptor-in-a-rat-stroke-ischemia-reperfusion-model
#11
Tao Tao, Jie Fu, Yong-Gang Liu, Zuo-Xiao Li, Xiao-Gang Li
OBJECTIVES: To investigate whether minocycline could inhibit neuroinflammation induced by microglia activation through suppression of adenosine A2Areceptor (A2AR)expression in rats after cerebral ischemia/reperfusion (I/R) injury. METHODS: Thirty male Sprageue-Dawley rats were randomly divided into 3 groups: sham group, I/R group and minocycline group. The rats were subjected to occlusion of the right middle cerebral artery (MCAO) for 2 h to establish stroke I/R model, and 3 mg/kg minocycline was injected intravenously immediately after reperfusion twice a day in minocycline group...
March 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/28609584/endothelial-nitric-oxide-synthase-inhibition-triggers-inflammatory-responses-in-the-brain-of-male-rats-exposed-to-ischemia-reperfusion-injury
#12
Rosaria Greco, Chiara Demartini, Anna Maria Zanaboni, Fabio Blandini, Diana Amantea, Cristina Tassorelli
Nitric oxide (NO) derived from endothelial NO synthase (eNOS) plays a role in preserving and maintaining the brain's microcirculation, inhibiting platelet aggregation, leukocyte adhesion, and migration. Inhibition of eNOS activity results in exacerbation of neuronal injury after ischemia by triggering diverse cellular mechanisms, including inflammatory responses. To examine the relative contribution of eNOS in stroke-induced neuroinflammation, we analyzed the effects of systemic treatment with l-N-(1-iminoethyl)ornithine (L-NIO), a relatively selective eNOS inhibitor, on the expression of MiR-155-5p, a key mediator of innate immunity regulation and endothelial dysfunction, in the cortex of male rats subjected to transient middle cerebral artery occlusion (tMCAo) followed by 24 hr of reperfusion...
June 13, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28608237/exogenous-adipokine-peptide-resistin-protects-against-focal-cerebral-ischemia-reperfusion-injury-in-mice
#13
Jiangtao Zhu, Di Wu, Chenyu Zhao, Man Luo, Ronald C Hamdy, Balvin H L Chua, Xingshun Xu, Zhigang Miao
Previous studies have demonstrated that plasma resistin levels were increased in patients with acute ischemic stroke. However, the role of resistin after ischemic brain injury is still unclear. In this study, we investigated the protective effects of resistin on cerebral ischemia/reperfusion injury in a middle cerebral artery occlusion mouse model. We found that resistin (i.c.v.) significantly reduced infarct volume and improved neurological deficits after 45 min of ischemia and 24 h of reperfusion. Furthermore, our data demonstrate that intraperitoneal administration of resistin (10 µg/kg body weight) also had protective effects on infarct volume, indicating the crossing of resistin through the impaired BBB after ischemia injury...
June 12, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28607351/early-oxygen-therapy-does-not-protect-the-brain-from-vasogenic-edema-following-acute-ischemic-stroke-in-adult-male-rats
#14
Elmira Pasban, Hamdollah Panahpour, Akbar Vahdati
Brain edema aggravates primary brain injury and increases its mortality rate after ischemic stroke. It is believed that normobaric oxygen therapy (NBO) may produce neuroprotective effects against ischemic stroke; however, reports have been controversial, and its effects on vasogenic brain edema as a major complication of brain ischemia have not been clarified. The present study investigates the effects of NBO on cerebral edema and blood - brain barrier integrity using rat model of ischemic stroke. Transient focal cerebral ischemia was induced in adult male Sprague-Dawley rats by left middle cerebral artery occlusion (MCAO) for 90 min followed by 24 h reperfusion...
June 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28602833/a-novel-il-1ra-pep-fusion-protein-with-enhanced-brain-penetration-ameliorates-cerebral-ischemia-reperfusion-injury-by-inhibition-of-oxidative-stress-and-neuroinflammation
#15
Dong-Dong Zhang, Min-Ji Zou, Ya-Tao Zhang, Wen-Liang Fu, Tao Xu, Jia-Xi Wang, Wen-Rong Xia, Zhi-Guang Huang, Xiang-Dong Gan, Xiao-Ming Zhu, Dong-Gang Xu
Neuroinflammation and oxidative stress are involved in cerebral ischemia-reperfusion, in which Interleukin 1 (IL-1), as an effective intervention target, is implicated. Interleukin-1 receptor antagonist (IL-1RA) is the natural inhibitor of IL-1, but blood-brain barrier (BBB) limits the brain penetration of intravenously administered IL-1RA, thereby restricting its therapeutic effect against neuroinflammation. In this study, we evaluated the potential effects of anti-inflammation and anti-oxidative stress of a novel protein IL-1RA-PEP, which fused IL-1RA with a cell penetrating peptide (CPP)...
June 8, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28596967/prdx6-upregulation-by-curcumin-attenuates-ischemic-oxidative-damage-via-sp1-in-rats-after-stroke
#16
Gongwei Jia, Botao Tan, Jingxi Ma, Lina Zhang, Xinhao Jin, Changqing Li
BACKGROUND: The role of Peroxiredoxin 6 (Prdx6) in brain ischemia remains unclear. Curcumin (Cur) treatment elicits neuroprotective effects against cerebral ischemic injury, and the associated mechanisms may involve Prdx6. In this study, we investigated whether Prdx6 and the transcription factor specific protein 1 (SP1) were involved in the antioxidant effect of Cur after stoke. METHODS: Focal cerebral ischemic injury was induced by transient middle cerebral artery occlusion for 2 hours in male Sprague-Dawley rats treated with or without Prdx6 siRNA...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28592261/trem2-protects-against-cerebral-ischemia-reperfusion-injury
#17
Rong Wu, Xiangpen Li, Pengfei Xu, Likui Huang, Jinping Cheng, Xiaolong Huang, Jingru Jiang, Long-Jun Wu, Yamei Tang
Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. Here, we found that the transcriptional and post-transcriptional levels of TREM2 were increased in cultured primary microglia after oxygen-glucose deprivation and reoxygenation and in the ischemic penumbra of the cerebral cortex after middle cerebral artery occlusion (MCAO) and reperfusion in mice...
June 7, 2017: Molecular Brain
https://www.readbyqxmd.com/read/28591739/improvement-of-mitochondrial-function-mediated-the-neuroprotective-effect-of-5-4-hydroxy-3-dimethoxybenzylidene-2-thioxo-4-thiazolidinone-in-rats-with-cerebral-ischemia-reperfusion-injuries
#18
Mingyang Wang, Lu Feng, Ji Zheng, Junya Liu, Shujie Fan, Jun Zhao, Nan Yang, Yanyong Liu, Zhanjun Yang, Caiying Ye, Pingping Zuo
Deficits in mitochondrial function is a critical inducement in the major pathways that drive neuronal cell death in ischemic process particularly. Drugs target to improve the mitochondrial function may be a feasible therapeutic choice in treatment with ischemic diseases. In the present study, we investigated whether 5-(4-hydroxy-3-dimethoxybenzylidene)-2-thioxo-4-thiazolidinone (RD-1), a compound derived from rhodanine, could protect against ischemic neuronal damage via improving mitochondrial function. We tested the neuroprotective effect of RD-1 both in rats modeled by middle cerebral artery occlusion reperfusion in vivo and in primary cortical neurons subjected to hypoxia/reperfusion injury in vitro...
May 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28591721/ginkgolide-k-attenuates-neuronal-injury-after-ischemic-stroke-by-inhibiting-mitochondrial-fission-and-gsk-3%C3%AE-dependent-increases-in-mitochondrial-membrane-permeability
#19
Xu Zhou, Hui-Ying Wang, Bin Wu, Cai-Yi Cheng, Wei Xiao, Zhen-Zhong Wang, Yu-Yu Yang, Ping Li, Hua Yang
Ginkgolide K (GK) belongs to the ginkgolide family of natural compounds found in Ginkgo biloba leaves, which have been used for centuries to treat cerebrovascular and cardiovascular diseases. We evaluated the protective effects of GK against neuronal apoptosis by assessing its ability to sustain mitochondrial integrity and function. Co-immunoprecipitation showed that Drp1 binding to GSK-3β was increased after an oxygen-glucose deprivation/reperfusion (OGD/R) insult in cultured neuroblastoma cells. This induced Drp1 and GSK-3β translocation to mitochondria and mitochondrial dysfunction, which was attenuated by GK...
May 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28569122/rationale-and-design-of-combination-of-an-immune-modulator-fingolimod-with-alteplase-bridging-with-mechanical-thrombectomy-in-acute-ischemic-stroke-famtais-trial
#20
Sheng Zhang, Ying Zhou, Ruiting Zhang, Meixia Zhang, Bruce Campbell, Longting Lin, Fu-Dong Shi, Min Lou
Rationale In acute ischemic stroke patients with large vessel occlusion, although reperfusion within 6 h after stroke onset using combined intravenous alteplase and mechanical thrombectomy (bridging therapy) can improve functional outcome, still approximately 50% patients suffer disability which may result from reperfusion injury. Proof-of-concept clinical trials have indicated that the sphingosine-1-phosphate receptor modulator fingolimod may be efficacious in attenuating brain inflammation and improving clinical outcomes in acute ischemic stroke patients as a single therapy beyond 4...
January 1, 2017: International Journal of Stroke: Official Journal of the International Stroke Society
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