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cerebral ischemia-reperfusion

Jingyan Zhao, Hongfeng Mu, Liqiang Liu, Xiaoyan Jiang, Di Wu, Yejie Shi, Rehana K Leak, Xunming Ji
Ischemic injury can be alleviated by the judicious use of hypothermia. However, the optimal regimens and the temporal kinetics of post-stroke neurovascular responses to hypothermic intervention have not been systematically studied. These gaps slow the clinical translation of hypothermia as an anti-stroke therapy. Here, we characterized the effects of transient selective brain hypothermia (TSBH) from the hyperacute to chronic stages of focal ischemia/reperfusion brain injury induced by transient middle cerebral artery occlusion in mice...
October 18, 2018: Journal of Cerebral Blood Flow and Metabolism
Yue-Yue Huang, Jian-Ming Wu, Tong Su, Song-Yue Zhang, Xiao-Ji Lin
Fasudil, a Rho-kinase inhibitor, has shown outstanding therapeutic effects against cerebral vasospasm after subarachnoid hemorrhage (SAH) in humans. Studies show various biological effects of fasudil in the cardiovascular system. We conducted a preclinical systematic review to determine the efficacy and possible mechanisms of fasudil on animal models of myocardial ischemia/reperfusion (I/R) injury. Nineteen studies involving 400 animals were identified after searching 8 databases for articles published till June 2018...
2018: Frontiers in Pharmacology
Abhishek Mukherjee, Sibani Sarkar, Sayantan Jana, Snehasikta Swarnakar, Nirmalendu Das
Cerebral ischemia-reperfusion (CIR) accelerates the progression of neurodegeneration by causing mitochondrial dysfunction to overproduce reactive oxygen species (ROS). Curcumin shows protective effects against CIR-induced oxidative damage. Free curcumin (FC) is effective at high doses due to its poor bioavailability. Also the blood-brain barrier (BBB) limits the passage of substances from circulation into the cerebral region. Thus, formulation of curcumin within polyethylene glycol (PEG)-ylated polylactide-co-glycolide (PLGA) nanoparticles (NC) was applied orally to aged rats to explore its role against CIR injury...
October 13, 2018: Brain Research
Seok Joon Won, Angela M Minnella, Long Wu, Claire H Eun, Eric Rome, Paco S Herson, Alisa E Shaw, James R Bamburg, Raymond A Swanson
Functional impairment after brain ischemia results in part from loss of neuronal spines and dendrites, independent of neuronal death. Cofilin-actin rods are covalently linked aggregates of cofilin-1 and actin that form in neuronal processes (neurites) under conditions of ATP depletion and oxidative stress, and which cause neurite degeneration if not disassembled. ATP depletion and oxidative stress occur with differing severity, duration, and time course in different ischemic conditions. Here we evaluated four mouse models of brain ischemia to define the conditions that drive formation of cofilin-actin rods...
2018: PloS One
Jiong Dai, Yong-Ming Qiu, Zheng-Wen Ma, Guo-Feng Yan, Jing Zhou, Shan-Quan Li, Hui Wu, Yi-Chao Jin, Xiao-Hua Zhang
Baicalin, a flavonoid compound from the root of the herb Scutellaria baicalensis Georgi, has been widely used to treat patients with inflammatory disease. The aim of this study was to assess the efficacy of baicalin in a rat model of focal cerebral ischemia. Adult male Sprague-Dawley rat models of cerebral artery occlusion were established and then randomly and equally divided into three groups: ischemia (cerebral ischemia and reperfusion), valproic acid (cerebral ischemia and reperfusion + three intraperitoneal injections of valproic acid; positive control), and baicalin (cerebral ischemia and reperfusion + intraperitoneal injection of baicalin for 21 days)...
December 2018: Neural Regeneration Research
Zheng Zhang, Jin-Long Yang, Lin-Lei Zhang, Zhen-Zhen Chen, Jia-Ou Chen, Yun-Gang Cao, Man Qu, Xin-Da Lin, Xun-Ming Ji, Zhao Han
We previously demonstrated that administering 2-(2-benzofuranyl)-2-imidazolin (2-BFI), an imidazoline I2 receptor agonist, immediately after ischemia onset can protect the brain from ischemic insult. However, immediate administration after stroke is difficult to realize in the clinic. Thus, the therapeutic time window of 2-BFI should be determined. Sprague-Dawley rats provided by Wenzhou Medical University in China received right middle cerebral artery occlusion for 120 minutes, and were treated with 2-BFI (3 mg/kg) through the caudal vein at 0, 1, 3, 5, 7, and 9 hours after reperfusion...
December 2018: Neural Regeneration Research
Yongying Hou, Ke Wang, Weijun Wan, Yue Cheng, Xia Pu, Xiufeng Ye
Ischemic stroke is a common disease with high mortality and morbidity worldwide. One of the important pathophysiological effects of ischemic stroke is apoptosis. A neuroprotective effect is defined as the inhibition of neuronal apoptosis to rescue or delay the infarction in the surviving ischemic penumbra. Resveratrol is a natural polyphenol that reportedly prevents cerebral ischemia injury by regulating the expression of PI3K/AKT/mTOR. Therefore, this study aimed to elucidate the neuroprotective effect of resveratrol on cerebral ischemia/reperfusion injury and to investigate the signaling pathways and mechanisms through which resveratrol regulates apoptosis in the ischemic penumbra...
September 2018: Genes & Diseases
Paloma González-Rodríguez, Irene F Ugidos, Diego Pérez-Rodríguez, Berta Anuncibay-Soto, María Santos-Galdiano, Enrique Font-Belmonte, José Manuel Gonzalo-Orden, Arsenio Fernández-López
Brain-derived neurotrophic factor (BDNF) is considered as a putative therapeutic agent against stroke. Since BDNF role on oxidative stress is uncertain, we have studied this role in a rat brain slice ischemia model, which allows BDNF reaching the neural parenchyma. Hippocampal and cerebral cortex slices were subjected to oxygen and glucose deprivation (OGD) and then returned to normoxic conditions (reperfusion-like, RL). OGD/RL increased a number of parameters mirroring oxidative stress in the hippocampus that were reduced by the BDNF presence...
October 14, 2018: Journal of Cellular Physiology
Xianzhang Zeng, Hongliang Ren, Yana Zhu, Ruru Zhang, Xinxin Xue, Tao Tao, Hongjie Xi
BACKGROUND/AIMS: Peri-operative cerebral ischemia reperfusion injury is one of the most serious peri-operative complications that can be aggravated in patients with diabetes. A previous study showed that microglia NOX2 (a NADPH oxidase enzyme) may play an important role in this process. Here, we investigated whether increased microglial derived gp91phox, also known as NOX2, reduced oxygen glucose deprivation (OGD) after induction of hyperglycemia (HG). METHODS: A rat neuronal-microglial in vitro co-culture model was used to determine the effects of gp91phox knockdown on OGD after HG using six treatment groups: A rat microglia and neuron co-culture model was established and divided into the following six groups: high glucose + scrambled siRNA transfection (HG, n = 5); HG + gp91phoxsiRNA transfection (HG-gp91siRNA, n = 5); oxygen glucose deprivation + scrambled siRNA transfection (OGD, n = 5); OGD + gp91phoxsiRNA transfection (OGD-gp91siRNA, n = 5); HG + OGD + scrambled siRNA transfection (HG-OGD, n = 5); and HG + OGD + gp91phoxsiRNA transfection (HG-OGD-gp91siRNA, n = 5)...
October 12, 2018: Cellular Physiology and Biochemistry
Chong-Jin Zhong, Miao-Miao Chen, Ming Lu, Jian-Hua Ding, Ren-Hong Du, Gang Hu
ATP-sensitive potassium (K-ATP) channels, coupling cell metabolism to cell membrane potential, are involved in brain diseases including stroke. Emerging evidence shows that astrocytes play important roles in the pathophysiology of cerebral ischemia. Kir6.1, a pore-forming subunit of K-ATP channel, is prominently expressed in astrocytes and participates in regulating its function. However, the exact role of astrocytic Kir6.1-containg K-ATP channel (Kir6.1/K-ATP) in ischemic stroke remains unclear. Here, we found that astrocytic Kir6...
October 10, 2018: Experimental Neurology
Hongyan Zhu, Rongrong Dai, Hao Fu, Qiang Meng
BACKGROUND: Blood-brain barrier (BBB) disruption plays a key role in the pathophysiology of acute ischemic stroke. Matrix metalloproteinases-2/9 (MMP-2/9) have been shown to participate in the disruption of the BBB and hemorrhagic transformation after cerebral ischemia. Toll-like receptor 2 (TLR2) may also be correlated with endothelial cell injury during ischemia-reperfusion events. However, the correlation between MMP-2/9 and TLR2 on endothelial cells after ischemia has not yet been evaluated...
October 8, 2018: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Bhakta Prasad Gaire, Mi-Ryoung Song, Ji Woong Choi
BACKGROUND: The pathogenic roles of receptor-mediated sphingosine 1-phosphate (S1P) signaling in cerebral ischemia have been evidenced mainly through the efficacy of FTY720 that binds non-selectively to four of the five S1P receptors (S1P1,3,4,5 ). Recently, S1P1 and S1P2 were identified as specific receptor subtypes that contribute to brain injury in cerebral ischemia; however, the possible involvement of other S1P receptors remains unknown. S1P3 can be the candidate because of its upregulation in the ischemic brain, which was addressed in this study, along with underlying pathogenic mechanisms...
October 10, 2018: Journal of Neuroinflammation
Yuxin Liu, Xianchuang Wu, Jihong An, Weiling Lv, Yanna Geng, Tingting Lou, Yongzhou Zhang
Oxidative stress has been implicated in the development of cerebral ischemia/reperfusion (I/R) injury. Glaucocalyxin B (GLB), one of five ent-kauranoid diterpenoids, was reported to possess neuroprotective activity. However, the effect of GLB on oxygen-glucose-deprivation/reperfusion (OGD/R)-induced cell injury in PC-12 cells has not been explored. PC-12 cells was treated with various concentrations of GLB (0, 2.5, 5 and 10 μM), and cell viability was detected using the MTT assay. PC-12 cells were pretreated with the indicated concentration of GLB (2...
October 10, 2018: Journal of Cellular Biochemistry
Nicola J Robertson, Kathryn Martinello, Ingran Lingam, Adnan Avdic-Belltheus, Christopher Meehan, Daniel Alonso-Alconada, Sara Ragab, Alan Bainbridge, Magda Sokolowska, Mohamed Tachrout, Benita Middleton, David Price, Mariya Hristova, Xavier Golay, Annamaria Soliani Raschini, Giancarlo Aquino, Nicola Pelizzi, Fabrizio Facchinetti
Therapeutic hypothermia is only partially protective for neonatal encephalopathy; there is an urgent need to develop treatments that augment cooling. Our objective was to assess safety, efficacy and pharmacokinetics of 5 and15 mg/kg/24 h melatonin (proprietary formulation) administered at 2 h and 26 h after hypoxia-ischemia (HI) with cooling in a piglet model. Following moderate cerebral HI, 30 piglets were eligible and randomized to: i) Hypothermia (33.5 °C, 2-26 h) and vehicle (HT + V;n = 13); b) HT and 5 mg/kg melatonin over 6 h at 2 h and 26 h after HI (HT + Mel-5;n = 4); c) HT and 15 mg/kg melatonin over 6 h at 2 h and 26 h after HI (HT + Mel-15;n = 13)...
October 6, 2018: Neurobiology of Disease
Amir Sedigh, Sofia Nordling, Fredrik Carlsson, Erik Larsson, Bo Norlin, Norbert Lübenow, Fredrik Lennmyr, Gunnar Tufveson, Peetra U Magnusson, Tomas Lorant
BACKGROUND: Previously we have been able to demonstrate the possibility of coating the inner surface of the renal arteries in porcine kidneys with a heparin conjugate during hypothermic machine perfusion (HMP). The purpose of this study was to assess the efficacy of this treatment in reducing early ischemia-reperfusion injury. METHOD: Brain death was induced in male landrace pigs by stepwise volume expansion of an epidural balloon catheter until negative cerebral perfusion pressure was obtained...
October 6, 2018: Transplantation
Hao Zhao, Wenlong Pan, Lihua Chen, Yongchun Luo, Ruxiang Xu
Mitochondrial fragmentation drastically regulates mitochondrial homeostasis in brain illness. However, the role of mitochondrial fragmentation in cerebral ischemia-reperfusion (IR) injury remains unclear. Nur77, a regulator of mitochondrial homeostasis, is associated with heart and liver IR injury, but its effects on mitochondrial function in cerebral IR injury has not been studied intensively. The aim of our study is to explore whether cerebral IR injury is modulated by Nur77 via modification of mitochondrial homeostasis...
October 8, 2018: Journal of Molecular Histology
Ji Wang, Zhimin Xu, Xiufen Chen, Yan Li, Chen Chen, Chongwu Wang, Jianwei Zhu, Zhaotao Wang, Wenjin Chen, Zongyu Xiao, Ruxiang Xu
Cerebral ischemia-reperfusion-induced microglial activation causes neuronal death through the release of inflammatory cytokines. Increasing evidence suggests that microRNAs (miRNAs) exert a neuroprotective effect by modulating the inflammatory process in cerebral ischemia-reperfusion injury. Furthermore, Toll-like receptor 4 (TLR4) is increasingly being considered to have a significant role in the regulation of inflammation. However, whether miRNAs mediate their neuroprotective effects by regulating TLR4-mediated inflammatory responses remains unknown...
October 3, 2018: Biochemical and Biophysical Research Communications
Maria Santos-Galdiano, Diego Perez-Rodriguez, Berta Anuncibay-Soto, Enrique Font-Belmonte, Irene F Ugidos, Carlos Cesar Perez-Garcia, Arsenio Fernandez-Lopez
BACKGROUND: Areas of selective neuronal loss (SNL) represent the first morphological signs of damage in the penumbra region and are considered putative targets for ischemic stroke therapy. Here we performed a novel assessment of measuring the effects of the anti-inflammatory agent, celecoxib, analyzing simultaneously the different neural populations (neurons, astrocytes and microglia cells) in SNL and non-SNL areas. METHODS: Rats were subjected to 1 hour of middle cerebral artery occlusion (MCAO) and treated with celecoxib 1 h and 24 h after ischemia...
October 5, 2018: Journal of Pharmacology and Experimental Therapeutics
Shameena Bake, Andre Okoreeh, Homa Khosravian, Farida Sohrabji
Our previous studies showed that Insulin-like Growth Factor (IGF)-1 reduced blood brain barrier permeability and decreased infarct volume caused by middle cerebral artery occlusion (MCAo) in middle aged female rats. Similarly, cultures of primary brain microvessel endothelial cells from middle-aged female rats and exposed to stroke-like conditions (oxygen glucose deprivation; OGD) confirmed that IGF-1 reduced dye transfer across this cell monolayer. Surprisingly, IGF-1 did not attenuate endothelial cell death caused by OGD...
October 1, 2018: Experimental Neurology
Cuiying Liu, Jian Yang, Chencheng Zhang, Xiaokun Geng, Heng Zhao
OBJECTIVE: Remote limb ischemic postconditioning (RIPostC) protects the brain from damage induced by transient focal ischemia/reperfusion. However, the underlying mechanism remains unclear. METHODS: RIPostC induced by 10 min of occlusion and another 10 min releasing of blood flow for three cycles in the hind limbs was performed immediately after the reperfusion in a focal ischemia mice model. Neurological scores, immune cell population in the blood, spleen and lymph node, and inflammatory factors in the blood and brain were analyzed 2 days after the reperfusion...
October 3, 2018: Neurological Research
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