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Specialty: Neurology
Condition: Stroke

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Total 100 results found since Jan 2013.

Nuclear translocation of histone deacetylase 4 induces neuronal death in stroke.
Abstract Mounting evidence suggests that epigenetic modifications play critical roles in the survival/death of stressed neurons. Chief among these modifications is the deacetylation of histones within the chromatin by histone deacetylases (HDACs). HDAC4 is highly expressed in neurons and is usually trapped in cytosol. However, tightly regulated signal-dependent shuttling of this molecule between cytosol and nucleus occurs. Here, we studied the intracellular trafficking of HDAC4 and regulatory mechanisms during stroke. HDAC4 translocated from the cytosol into the nucleus of neurons in response to stroke induced by ...
Source: Neurobiology of Disease - March 8, 2016 Category: Neurology Authors: Yuan H, Denton K, Liu L, Li XJ, Benashski S, McCullough L, Li J Tags: Neurobiol Dis Source Type: research

Lipoxin A4 Reduces Inflammation Through Formyl Peptide Receptor 2/p38 MAPK Signaling Pathway in Subarachnoid Hemorrhage Rats Basic Sciences
Conclusions— Exogenous LXA4 inhibited inflammation by activating FPR2 and inhibiting p38 after SAH. LXA4 may serve as an alternative treatment to relieve early brain injury after SAH.
Source: Stroke - January 25, 2016 Category: Neurology Authors: Guo, Z., Hu, Q., Xu, L., Guo, Z.-N., Ou, Y., He, Y., Yin, C., Sun, X., Tang, J., Zhang, J. H. Tags: Animal Models of Human Disease Basic Sciences Source Type: research

Leukemia Inhibitory Factor Protects Neurons from Ischemic Damage via Upregulation of Superoxide Dismutase 3
Abstract Leukemia inhibitory factor (LIF) has been shown to protect oligodendrocytes from ischemia by upregulating endogenous antioxidants. The goal of this study was to determine whether LIF protects neurons during stroke by upregulating superoxide dismutase 3 (SOD3). Animals were administered phosphate-buffered saline (PBS) or 125 μg/kg LIF at 6, 24, and 48 h after middle cerebral artery occlusion or sham surgery. Neurons were isolated from rat pups on embryonic day 18 and used between 7 and 15 days in culture. Cells were treated with LIF and/or 10 μM Akt inhibitor IV with PBS and 0.1 % DMSO acting as veh...
Source: Molecular Neurobiology - January 9, 2016 Category: Neurology Source Type: research

Upregulating the Expression of Survivin-HBXIP Complex Contributes to the Protective Role of IMM-H004 in Transient Global Cerebral Ischemia/Reperfusion
Abstract IMM-H004, a 3-piperazinylcoumarin compound derived from coumarin, has been proved effective against CA1 cell loss and spatial learning impairments resulting from transient global ischemia/reperfusion (TGCI/R), while the mechanism is still largely unknown. Here, we confirmed that treatment of rats with IMM-H004 immediately after TGCI/R ameliorated delayed neuronal death (DND) in the CA1 of hippocampus and cortex. Further study suggested that IMM-H004 contributed to the expression of antiapoptotic protein survivin through the activation of PI3K-dependent protein kinase B (PKB/Akt), which led to the phosphor...
Source: Molecular Neurobiology - January 7, 2016 Category: Neurology Source Type: research

Cytosolic phospholipase A 2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway
Conclusions: In summary, the results in this study demonstrated the role of cPLA 2 in microglial activation with metabolic links to oxidative and inflammatory responses, and this was in part regulated by the AA metabolic pathways, namely the LOXs. Further studies with targeted inhibition of cPLA 2 /LOX in microglia during neuroinflammatory conditions can be valuable to investigate the therapeutic potential in ameliorating neurological disease pathology.
Source: Journal of Neuroinflammation - October 31, 2015 Category: Neurology Authors: Dennis ChuangAgnes SimonyiPaul KotzbauerZezong GuGrace Sun Source Type: research

Autophagy protects Human Brain Microvascular Endothelial Cells against Methylglyoxal‐induced Injuries: in parallel with Cerebral Ischemic Model in Diabetic Rats
This article is protected by copyright. All rights reserved.
Source: Journal of Neurochemistry - August 1, 2015 Category: Neurology Authors: Lili Fang, Xue Li, Yinbo Zhong, Jing Yu, Lina Yu, Haibin Dai, Min Yan Tags: Original Article Source Type: research

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

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

Neuroprotective Role of an N-acetyl Serotonin Derivative via Activation of Tropomyosin-related Kinase Receptor B after Subarachnoid Hemorrhage in a Rat Model.
This study is to investigate a potential role of HIOC on ameliorating early brain injury after experimental subarachnoid hemorrhage (SAH). One hundred and fifty-six adult male Sprague-Dawley rats were used. SAH model was induced by endovascular perforation. TrkB small interfering RNA (siRNA) or scramble siRNA was injected intracerebroventricularly 24hours before SAH. HIOC was administrated intracerebroventricularly 3hours after SAH and compared with brain-derived neurotrophic factor (BDNF). SAH grade and neurologic scores were evaluated for the outcome study. For the mechanism study, the expression of TrkB, phosphorylated ...
Source: Neurobiology of Disease - April 8, 2015 Category: Neurology Authors: Tang J, Hu Q, Chen Y, Liu F, Zheng Y, Tang J, Zhang J, Zhang JH Tags: Neurobiol Dis Source Type: research

17{beta}-Estradiol Attenuates Hematoma Expansion Through Estrogen Receptor {alpha}/Silent Information Regulator 1/Nuclear Factor-kappa B Pathway in Hyperglycemic Intracerebral Hemorrhage Mice Basic Sciences
Conclusions— E2 treatment prevented hyperglycemia-enhanced HE and improved neurological deficits in ICH mice mediated by ERα/Sirt1/nuclear factor-kappa B pathway. E2 may serve as an alternative treatment to decrease early HE after ICH.
Source: Stroke - January 26, 2015 Category: Neurology Authors: Zheng, Y., Hu, Q., Manaenko, A., Zhang, Y., Peng, Y., Xu, L., Tang, J., Tang, J., Zhang, J. H. Tags: Animal models of human disease, Neuroprotectors Basic Sciences 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

Inhibition of thioredoxin-1 with siRNA exacerbates apoptosis by activating the ASK1-JNK/p38 pathway in brain of a stroke model rats.
Abstract Apoptosis is critical for the development of cerebral ischemia/reperfusion injury. Thioredoxin-1(Trx-1) protein has been reported to have anti-apoptotic effects in a variety of cell types, and it has been implicated in brain injury after middle cerebral artery occlusion (MCAO). Thus, we studied the effects of Trx1 silencing after MCAO in rats and examined whether inhibition of endogenous Trx1 could increase tissue levels of apoptosis. Male Sprague-Dawley rats (N=170) were subjected to 1h of middle cerebral arterial occlusion followed by 24h of reperfusion. Trx1 siRNAs were injected into rat brains 24h pri...
Source: Brain Research - December 22, 2014 Category: Neurology Authors: Wu X, Li L, Zhang L, Wu J, Zhou Y, Zhou Y, Zhao Y, Zhao J Tags: Brain Res 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