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Condition: Ischemic Stroke

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Total 193 results found since Jan 2013.

Osteopontin Mediates Hyperbaric Oxygen Preconditioning-Induced Neuroprotection Against Ischemic Stroke
Abstract Neurosurgical operations may result in surgical injury which would lead to postoperative neurological deficits. Hyperbaric oxygen preconditioning (HBO-PC) may be beneficial for such people. However, the exact mechanism underlying HBO-PC is not well known yet. The aim of this study is to explore the role of osteopontin (OPN) in HBO-PC-induced neuroprotection. The study consisted of two experiments. In experiment 1, Sprague Dawley (SD) rats were divided into four groups: sham group, HBO-PC sham group, stroke group, and HBO-PC group (HBO-PC + stroke). The animals in the second experiment were randomly a...
Source: Molecular Neurobiology - July 21, 2015 Category: Neurology Source Type: research

Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis.
This study was aimed to investigate whether knockdown of Id2 in neuronal cells could protect them from hypoxic and ischemic injury both in vitro and in vivo. Flow cytometric analysis was employed to assess neuronal apoptosis in CoCl2-treated neuroblastoma B35 cells engineered to overexpress or knockdown Id2 expression. In vivo knockdown of Id2 was performed in Sprague-Dawley rats by a single intracerebroventricular injection of Cy3-labeled and cholesterol-modified Id2-siRNA. We found that knockdown of Id2 attenuated H/I-induced neuronal apoptosis in vitro while overexpression of Id2 produced an opposite effect. In a rat mo...
Source: Behavioural Brain Research - July 14, 2015 Category: Neurology Authors: Guo L, Yang X, Lin X, Lin Y, Shen L, Nie Q, Ren L, Guo Q, Que S, Qiu Y Tags: Behav Brain Res Source Type: research

PPAR-γ Ameliorates Neuronal Apoptosis and Ischemic Brain Injury via Suppressing NF-κB-Driven p22phox Transcription
Abstract Peroxisome proliferator-activated receptor-gamma (PPAR-γ), a stress-induced transcription factor, protects neurons against ischemic stroke insult by reducing oxidative stress. NADPH oxidase (NOX) activation, a major driving force in ROS generation in the setting of reoxygenation/reperfusion, constitutes an important pathogenetic mechanism of ischemic brain damage. In the present study, both transient in vitro oxygen-glucose deprivation and in vivo middle cerebral artery (MCA) occlusion-reperfusion experimental paradigms of ischemic neuronal death were used to investigate the interaction between PPAR-γ a...
Source: Molecular Neurobiology - June 24, 2015 Category: Neurology Source Type: research

Neuroprotection of Sanhua Decoction against Focal Cerebral Ischemia/Reperfusion Injury in Rats through a Mechanism Targeting Aquaporin 4.
In conclusion, SHD exerted neuroprotection against focal cerebral I/R injury in rats mainly through a mechanism targeting AQP4. PMID: 26089944 [PubMed]
Source: Evidence-based Complementary and Alternative Medicine - June 21, 2015 Category: Complementary Medicine Tags: Evid Based Complement Alternat Med Source Type: research

Diallyl trisufide protects against oxygen glucose deprivation -induced apoptosis by scavenging free radicals via the PI3K/Akt -mediated Nrf2/HO-1 signaling pathway in B35 neural cells.
Abstract Oxidative stress contributes to development of ischemic brain damage. Many antioxidants have been proven effective in ameliorating cerebral ischemia injury by inhibiting oxidative stress. DATS, an organosulfuric component of garlic oil, exhibits antioxidative effects. In present study, we used OGD model to investigate the neuroprotective effects of DATS and the mechanisms related to these effects. B35 neural cells exposed to OGD caused a decrease in cell viability and increases in the percentage of apoptotic cells and the level of intracellular cleaved caspase-3, all of which were markedly attenuated by D...
Source: Brain Research - April 17, 2015 Category: Neurology Authors: Li Li G, Wang BA, Hua Xu X, Qin Y, Rong Bai S, Rong J, Deng T, Li Q Tags: Brain Res Source Type: research

Dioscin ameliorates cerebral ischemia/reperfusion injury through the downregulation of TLR4 signaling via HMGB-1 inhibition.
Abstract We previously reported the promising effect of dioscin against hepatic ischemia /reperfusion (I/R) injury, but its effect on cerebral I/R injury remains unknown. In this work, an in vitro oxygen-glucose deprivation and reoxygenation (OGD/R) model and an in vivo middle cerebral artery occlusion (MCAO) model were used. The results indicated that dioscin clearly protected PC12 cells and primary cortical neurons against OGD/R insult and significantly prevented cerebral I/R injury. Further research demonstrated that dioscin-induced neuroprotection was accompanied by a significant inhibition in the expression a...
Source: Free Radical Biology and Medicine - March 12, 2015 Category: Biology Authors: Tao X, Sun X, Yin L, Han X, Xu L, Qi Y, Xu Y, Li H, Lin Y, Liu K, Peng J Tags: Free Radic Biol Med Source Type: research

i-Fect Delivers siRNA in vitro and in vivo
In this study data suggest the protective effects of EPO on NUV injuries are highly associated with the increase of p-Cx43, which improves GJIC to reduce neurotoxic substances: Ziyi Zhoua, Xiaobai Weib, Jun Xiang, Junpeng Gao, Lixin Wang, Jinsong You, Yefeng Cai , Dingfang Caid. Protection of erythropoietin against ischemic neurovascular unit injuries through the effects of connexin43. Biochemical and Biophysical Research Communications. doi:10.1016/j.bbrc.2015.02...The strands were incubated at 90°C for 5 min and then at 37°C for 1 h. SiRNA was prepared immediately before administration by mixing the RNA solution (1 μg...
Source: Neuromics - February 21, 2015 Category: Neuroscience Tags: Cerebral Ischemia Connexin 43 Delivering siRNA to the CNS EPO HDAC2 i-Fect Stroke Source Type: news

DDR1 may play a key role in destruction of the blood–brain barrier after cerebral ischemia–reperfusion
Publication date: Available online 25 January 2015 Source:Neuroscience Research Author(s): Mingxia Zhu , Dong Xing , Zhihong Lu , Yanhong Fan , Wugang Hou , Hailong Dong , Lize Xiong , Hui Dong Discoidin domain receptor 1 (DDR1) has been shown to mediate matrix metalloproteinase-9 (MMP-9) secretions and degrade all extracellular matrix compounds in mammalian tumor cells. We hypothesized that DDR1 expression will be elevated and the blood–brain barrier (BBB) will be damaged after focal cerebral ischemia in rats. Inhibiting DDR1 expression can alleviate BBB disruption and cerebral ischemic damage via down-regulation of M...
Source: Neuroscience Research - January 30, 2015 Category: Neuroscience Source Type: research

MicroRNA-424 Protects Against Focal Cerebral Ischemia and Reperfusion Injury in Mice by Suppressing Oxidative Stress Basic Sciences
Conclusions— MiR-424 protects against transient cerebral ischemia/reperfusion injury by inhibiting oxidative stress.
Source: Stroke - January 26, 2015 Category: Neurology Authors: Liu, P., Zhao, H., Wang, R., Wang, P., Tao, Z., Gao, L., Yan, F., Liu, X., Yu, S., Ji, X., Luo, Y. Tags: Acute Cerebral Infarction Basic Sciences Source Type: research

Cofilin Inhibition Restores Neuronal Cell Death in Oxygen–Glucose Deprivation Model of Ischemia
Abstract Ischemia is a condition associated with decreased blood supply to the brain, eventually leading to death of neurons. It is associated with a diverse cascade of responses involving both degenerative and regenerative mechanisms. At the cellular level, the changes are initiated prominently in the neuronal cytoskeleton. Cofilin, a cytoskeletal actin severing protein, is known to be involved in the early stages of apoptotic cell death. Evidence supports its intervention in the progression of disease states like Alzheimer’s and ischemic kidney disease. In the present study, we have hypothesized the possible i...
Source: Molecular Neurobiology - December 20, 2014 Category: Neurology Source Type: research

Critical role of extracellularly secreted neuronal pentraxin 1 in ischemic neuronal death
Conclusions: Collectively, our results demonstrate that extracellular release of NP1 promote hypoxic-ischemic neuronal death possible via surface clustering with GluR1 at synaptic sites and that NP1, not its family member NP2, is involved in the neuronal death mechanisms.
Source: BMC Neuroscience - December 20, 2014 Category: Neuroscience Authors: Shabarish ThatipamulaMir Hossain Source Type: research

Candesartan stimulates reparative angiogenesis in ischemic retinopathy model: role of hemeoxygenase-1 (HO-1)
Abstract Ischemic diseases such as stroke and proliferative retinopathy are characterized by hypoxia-driven release of angiogenic factors such as vascular endothelial growth factor (VEGF). However, revascularization of the ischemic areas is inadequate, resulting in impaired neuro-vascular function. We aim to examine the vascular protective effects of candesartan, an angiotensin receptor blocker, in an ischemic retinopathy mouse model. Vascular density, number of tip cells, and perfusions of capillaries were assessed. Activation of Muller glial cells and levels of peroxynitrite, VEGF, VEGFR2, inducible nitric o...
Source: Angiogenesis - November 25, 2014 Category: Molecular Biology Source Type: research

Recombinant Milk Fat Globule-EGF Factor-8 Reduces Oxidative Stress via Integrin {beta}3/Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase Pathway in Subarachnoid Hemorrhage Rats Basic Sciences
Conclusions— Recombinant MFGE8 attenuated oxidative stress that may be mediated by integrin β3/nuclear factor erythroid 2–related factor 2/HO pathway after SAH. Recombinant MFGE8 may serve as an alternative treatment to ameliorate early brain injury for SAH patients.
Source: Stroke - November 24, 2014 Category: Neurology Authors: Liu, F., Hu, Q., Li, B., Manaenko, A., Chen, Y., Tang, J., Guo, Z., Tang, J., Zhang, J. H. Tags: Animal models of human disease, Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage Basic Sciences Source Type: research

Remote Ischemic Postconditioning Alleviates Cerebral Ischemic Injury by Attenuating Endoplasmic Reticulum Stress-Mediated Apoptosis
Abstract Remote ischemic postconditioning (RIPostC) has been proved to protect the brain from stroke, but the precise mechanism remains not fully understood. In the present study, we aimed to investigate whether RIPostC attenuates cerebral ischemia-reperfusion injury by abating endoplasmic reticulum (ER) stress response. CHOP, a multifunctional transcription factor in ER stress, regulates the expression of genes related to apoptosis, such as Bim and Bcl-2. Male SD rats were subjected to right middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion, and RIPostC was induced by three cycles of 10 m...
Source: Translational Stroke Research - October 30, 2014 Category: Neurology Source Type: research