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Source: Neurochemical Research

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Total 300 results found since Jan 2013.

MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway.
Abstract The present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In v...
Source: Neurochemical Research - June 13, 2016 Category: Neuroscience Authors: Wang P, Liang X, Lu Y, Zhao X, Liang J Tags: Neurochem Res Source Type: research

Protective Effect of Aliskiren in Experimental Ischemic Stroke: Up-Regulated p-PI3K, p-AKT, Bcl-2 Expression, Attenuated Bax Expression.
This study aimed to investigate the role of ALK and its potential mechanism in cerebral ischemia. C57/BL6 mice were subjected to transient middle cerebral artery occlusion (tMCAO) and treated for 5 days with Vehicle or ALK (10 or 25 mg/kg per day via intragastric administration), whereas Sham-operated animals served as controls. Treatment with ALK significantly improved neurological deficits, infarct volume, brain water content and Nissl bodies after stroke (P < 0.05), which did not affect systemic blood pressure. Furthermore, the protection of ALK was also related to decreased levels of apoptosis in mice by enhance...
Source: Neurochemical Research - May 13, 2016 Category: Neuroscience Authors: Miao J, Wang L, Zhang X, Zhu C, Cui L, Ji H, Liu Y, Wang X Tags: Neurochem Res Source Type: research

Ornithine and Homocitrulline Impair Mitochondrial Function, Decrease Antioxidant Defenses and Induce Cell Death in Menadione-Stressed Rat Cortical Astrocytes: Potential Mechanisms of Neurological Dysfunction in HHH Syndrome.
Abstract Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is caused by deficiency of ornithine translocase leading to predominant tissue accumulation and high urinary excretion of ornithine (Orn), homocitrulline (Hcit) and ammonia. Although affected patients commonly present neurological dysfunction manifested by cognitive deficit, spastic paraplegia, pyramidal and extrapyramidal signs, stroke-like episodes, hypotonia and ataxia, its pathogenesis is still poorly known. Although astrocytes are necessary for neuronal protection. Therefore, in the present study we investigated the effects of Orn and ...
Source: Neurochemical Research - May 8, 2016 Category: Neuroscience Authors: Zanatta Â, Rodrigues MD, Amaral AU, Souza DG, Quincozes-Santos A, Wajner M Tags: Neurochem Res Source Type: research

Treatment with Isorhamnetin Protects the Brain Against Ischemic Injury in Mice.
In conclusion, treatment with isorhamnetin protected the brain against ischemic injury in mice. Isorhamnetin could thus be envisaged as a countermeasure for ischemic stroke but remains to be tested in humans. PMID: 27161367 [PubMed - as supplied by publisher]
Source: Neurochemical Research - May 8, 2016 Category: Neuroscience Authors: Zhao JJ, Song JQ, Pan SY, Wang K Tags: Neurochem Res Source Type: research

Blocking Sympathetic Nervous System Reverses Partially Stroke-Induced Immunosuppression but does not Aggravate Functional Outcome After Experimental Stroke in Rats.
This study suggests that pharmacological SNS inhibition dose not aggravate functional outcome after stroke. Stroke-induced immunosuppression may be involved in the SNS-β-arrestin2-NF-κB pathway. PMID: 27059792 [PubMed - as supplied by publisher]
Source: Neurochemical Research - April 7, 2016 Category: Neuroscience Authors: Deng QW, Yang H, Yan FL, Wang H, Xing FL, Zuo L, Zhang HQ Tags: Neurochem Res Source Type: research

Uptake and Toxicity of Hemin and Iron in Cultured Mouse Astrocytes.
Abstract Hemin is a breakdown product of the blood protein, hemoglobin and is responsible for much of the secondary damage caused following a hemorrhagic stroke. Hemin is toxic to cultured astrocytes and it is thought that this toxicity is due to iron that is liberated when hemin is degraded. However, free iron applied to astrocytes is not toxic and the reason for this discrepancy is unknown. The present study exposed primary astrocyte cultures from neonatal mice to hemin-iron (25 µM hemin) or non-hemin iron (25 µM ferric ammonium citrate; FAC) for 12 or 24 h. Perls' and Turnbull's staining, as well as measur...
Source: Neurochemical Research - December 22, 2015 Category: Neuroscience Authors: Owen JE, Bishop GM, Robinson SR Tags: Neurochem Res Source Type: research

Cerebral Response to Peripheral Challenge with a Viral Mimetic.
Abstract It has been well established that peripheral inflammation resulting from microbial infections profoundly alters brain function. This review focuses on experimental systems that model cerebral effects of peripheral viral challenge. The most common models employ the induction of the acute phase response via intraperitoneal injection of a viral mimetic, polyinosinic-polycytidylic acid (PIC). The ensuing transient surge of blood-borne inflammatory mediators induces a "mirror" inflammatory response in the brain characterized by the upregulated expression of a plethora of genes encoding cytokines, chemokines an...
Source: Neurochemical Research - November 2, 2015 Category: Neuroscience Authors: Konat G Tags: Neurochem Res Source Type: research

Rhynchophylline Protects Against the Amyloid β-Induced Increase of Spontaneous Discharges in the Hippocampal CA1 Region of Rats.
Abstract Accumulated soluble amyloid β (Aβ)-induced aberrant neuronal network activity has been recognized as a key causative factor leading to cognitive deficits which are the most outstanding characteristic of Alzheimer's disease (AD). As an important structure associated with learning and memory, the hippocampus is one of the brain regions that are impaired very early in AD, and the hippocampal CA1 region is selectively vulnerable to soluble Aβ oligomers. Our recent study showed that soluble Aβ1-42 oligomers induced hyperactivity and perturbed the firing patterns in hippocampal neurons. Rhynchophylline (RIN...
Source: Neurochemical Research - October 6, 2015 Category: Neuroscience Authors: Shao H, Mi Z, Ji WG, Zhang CH, Zhang T, Ren SC, Zhu ZR Tags: Neurochem Res Source Type: research

Taurine Protected Against the Impairments of Neural Stem Cell Differentiated Neurons Induced by Oxygen-Glucose Deprivation.
Abstract Cell transplantation of neural stem cells (NSCs) is a promising approach for neurological recovery both structurally and functionally. However, one big obstacle is to promote differentiation of NSCs into neurons and the followed maturation. In the present study, we aimed to investigate the protective effect of taurine on the differentiation of NSCs and subsequent maturation of their neuronal lineage, when exposed to oxygen-glucose deprivation (OGD). The results suggested that taurine (5-20 mM) promoted the viability and proliferation of NSCs, and it protected against 8 h of OGD induced impairments. Furt...
Source: Neurochemical Research - September 28, 2015 Category: Neuroscience Authors: Xiao B, Liu H, Gu Z, Liu S, Ji C Tags: Neurochem Res Source Type: research

Proteinase 3 Induces Neuronal Cell Death Through Microglial Activation.
Abstract Proteinase 3 (PR3) is released from neutrophil granules and is involved in the inflammatory process. PR3 is implicated in antimicrobial defense and cell death, but the exact role of PR3 in the brain is less defined. Microglia is the major immune effector cells in the CNS and is activated by brain injury. In the present study, the effect of PR3 on glial activation was investigated. Microglial activation was assessed by the intracellular level of reactive oxygen species and expression of inflammatory cytokines. The conditioned media from activated microglia by PR3 was used for measuring the neurotoxic effec...
Source: Neurochemical Research - September 8, 2015 Category: Neuroscience Authors: Cho KS, Lee EJ, Kim JN, Choi JW, Kim HY, Han SH, Ryu JH, Cheong JH, Shin CY, Kwon KJ Tags: Neurochem Res Source Type: research

Concentration-Dependent Dual Role of Thrombin in Protection of Cultured Rat Cortical Neurons.
We examined thrombin's effect on neurites by quantitative analysis of fluorescently labeled neurons. To characterize thrombin's effects on neuron survival, we spectrophotometrically measured changes in enzymatic activity. Using receptor agonists and thrombin inhibitors, we separately examined the role of thrombin and its receptor in neuroprotection. We found that low concentrations of thrombin (1 nM) enhances neurite growth and branching, neuron viability, and protects against excitotoxic damage. In contrast, higher concentrations of thrombin (100 nM) are potentially detrimental to neuronal health as evidenced by inhibit...
Source: Neurochemical Research - September 5, 2015 Category: Neuroscience Authors: García PS, Ciavatta VT, Fidler JA, Woodbury A, Levy JH, Tyor WR Tags: Neurochem Res Source Type: research

New Insights into the Roles of Nogo-A in CNS Biology and Diseases.
Abstract Nogos have become a hot topic for its well-known number Nogo-A's big role in clinical matters. It has been recognized that the expression of Nogo-A and the receptor NgR1 inhibit the neuron's growth after CNS injuries or the onset of the MS. The piling evidence supports the notion that the Nogo-A is also involved in the synaptic plasticity, which was shown to negatively regulate the strength of synaptic transmission. The occurrence of significant schizophrenia-like behavioral phenotypes in Nogo-A KO rats also added strong proof to this conclusion. This review mainly focuses on the structure of Nogo-A and i...
Source: Neurochemical Research - August 13, 2015 Category: Neuroscience Authors: Sui YP, Zhang XX, Lu JL, Sui F Tags: Neurochem Res Source Type: research

Critical Evaluation of the Changes in Glutamine Synthetase Activity in Models of Cerebral Stroke.
Abstract The following article addresses some seemingly paradoxical observations concerning cerebral glutamine synthetase in ischemia-reperfusion injury. In the brain, this enzyme is predominantly found in astrocytes and catalyzes part of the glutamine-glutamate cycle. Glutamine synthetase is also thought to be especially sensitive to inactivation by the oxygen- and nitrogen-centered radicals generated during strokes. Despite this apparent sensitivity, glutamine synthetase specific activity is elevated in the affected tissues during reperfusion. Given the central role of the glutamine-glutamate cycle in the brain...
Source: Neurochemical Research - August 2, 2015 Category: Neuroscience Authors: Jeitner TM, Battaile K, Cooper AJ Tags: Neurochem Res Source Type: research

T Cells and Cerebral Ischemic Stroke.
Abstract Stroke results in cerebral inflammation that causes brain injury and triggers immunodepression, resulting in an increased incidence of morbidity and mortality secondary to remote infection. It is well known that T cells modulate brain inflammation after ischemic stroke, and targeting T cells may be an innovative therapeutic strategy for stroke treatment. T cell deficiency is neuro-protective, but the observed protective effects differ between ischemic models. Recent studies suggest different T cell subsets may have distinct effects on the injured brain. In addition to their role in cerebral inflammation, ...
Source: Neurochemical Research - July 29, 2015 Category: Neuroscience Authors: Gu L, Jian Z, Stary C, Xiong X Tags: Neurochem Res Source Type: research

Neuroprotective Effects of (-)-Epigallocatechin-3-Gallate Against Focal Cerebral Ischemia/Reperfusion Injury in Rats Through Attenuation of Inflammation.
Abstract Stroke is the second leading cause of death among adults worldwide. (-)-Epigallocatechin-3-gallate (EGCG) has been demonstrated to exhibit neuroprotective functions in cerebral ischemia/reperfusion injury. However, the underlying mechanisms in this process and its contribution to the protection function remain unknown. The current study examined the neuroprotective effects of EGCG after transient middle cerebral artery occlusion (tMCAO) in rats. tMCAO for 120 min was induced in male Sprague-Dawley rats treated with EGCG (50 mg/kg, i.p.) or Vehicle immediately after reperfusion. Neurological score, infar...
Source: Neurochemical Research - July 22, 2015 Category: Neuroscience Authors: Zhang F, Li N, Jiang L, Chen L, Huang M Tags: Neurochem Res Source Type: research