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Source: Molecular Neurobiology
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Total 278 results found since Jan 2013.
LncRNA XIST Exacerbates Oxygen-Glucose Deprivation/Reoxygenation-Induced Cerebral Injury Through the miR-25-3p/TRAF3 Axis
AbstractIschemic stroke causes lethal damage to the brain. Identifying key regulators of OGD/R-induced cerebral injury is important for developing novel therapies for ischemic stroke. HMC3 and SH-SY5Y cells were treated with OGD/R as anin vitro ischemic stroke model. Cell viability and apoptosis were determined via CCK-8 assay and flow cytometry. Inflammatory cytokines were examined by ELISA. Luciferase activity was measured for evaluating the interaction of XIST, miR-25-3p, and TRAF3. Bcl-2, Bax, Bad, cleaved-caspase 3, total caspase 3, and TRAF3 were detected via western blotting. HMC3 and SH-SY5Y cells showed increased ...
Source: Molecular Neurobiology - September 7, 2023 Category: Neurology Source Type: research
Combination of HBO and Memantine in Focal Cerebral Ischemia: Is There a Synergistic Effect?
In this study, we investigated whether or not MEM could prolong the narrow therapeutic window of HBO treatment. Transient focal cerebral ischemia was induced in male Sprague–Dawley rats by middle cerebral artery occlusion (MCAO) for 120 min. MCAO produced neurobehavioral deficits, increased infarction volume, increased Evans blue (EB) content and levels of pro-inflammatory factors, as well as depleted glutathione (GSH), and reduced catalase (CAT) and superoxide dismutase (SOD) activity in the ischemic ipsilateral hemisphere. The combination of 5 mg/kg MEM treatment 15 min after the onset of ischemic event and HBO ther...
Source: Molecular Neurobiology - October 30, 2014 Category: Neurology Source Type: research
From Chemotherapy-Induced Emesis to Neuroprotection: Therapeutic Opportunities for 5-HT 3 Receptor Antagonists
Abstract
5-HT3 receptor antagonists are extensively used as efficacious agents in counteracting chemotherapy-induced emesis. Recent investigations have shed light on other potential effects (analgesic, anxiolytic, and anti-psychotic). Some studies have reported neuroprotective properties for the 5-HT3 receptor antagonists in vitro and in vivo. When administered to Aβ-challenged rat cortical neurons, 5-HT3 receptor antagonists substantially abated apoptosis, elevation of cytosolic Ca2, glutamate release, reactive oxygen species (ROS) generation, and caspase-3 activity. In addition, in vivo studies show that 5-HT3 ...
Source: Molecular Neurobiology - November 7, 2014 Category: Neurology Source Type: research
Crosstalk Between Endoplasmic Reticulum Stress, Oxidative Stress, and Autophagy: Potential Therapeutic Targets for Acute CNS Injuries
Abstract
Endoplasmic reticulum (ER) stress induces a variety of neuronal cell death pathways that play a critical role in the pathophysiology of stroke. ER stress occurs when unfolded/misfolded proteins accumulate and the folding capacity of ER chaperones exceeds the capacity of ER lumen to facilitate their disposal. As a consequence, a complex set of signaling pathways will be induced that transmit from ER to cytosol and nucleus to compensate damage and to restore the normal cellular homeostasis, collectively known as unfolded protein response (UPR). However, failure of UPR due to severe or prolonged stress leads...
Source: Molecular Neurobiology - December 8, 2014 Category: Neurology Source Type: research
N -Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution
Abstract
Inflammation is fundamentally a protective cellular response aimed at removing injurious stimuli and initiating the healing process. However, when prolonged, it can override the bounds of physiological control and becomes destructive. Inflammation is a key element in the pathobiology of chronic pain, neurodegenerative diseases, stroke, spinal cord injury, and neuropsychiatric disorders. Glia, key players in such nervous system disorders, are not only capable of expressing a pro-inflammatory phenotype but respond also to inflammatory signals released from cells of immune origin such as mast cells. Chronic ...
Source: Molecular Neurobiology - June 8, 2015 Category: Neurology Source Type: research
Cerebral Ischemic Preconditioning: the Road So Far…
Abstract
Cerebral preconditioning constitutes the brain’s adaptation to lethal ischemia when first exposed to mild doses of a subtoxic stressor. The phenomenon of preconditioning has been largely studied in the heart, and data from in vivo and in vitro models from past 2–3 decades have provided sufficient evidence that similar machinery exists in the brain as well. Since preconditioning results in a transient protective phenotype labeled as ischemic tolerance, it can open many doors in the medical warfare against stroke, a debilitating cerebrovascular disorder that kills or cripples thousands of people worldw...
Source: Molecular Neurobiology - June 17, 2015 Category: Neurology Source Type: research
Chronic Metformin Preconditioning Provides Neuroprotection via Suppression of NF-κB-Mediated Inflammatory Pathway in Rats with Permanent Cerebral Ischemia
In this study, we tested the hypothesis that chronic preconditioning with metformin conferred neuroprotection via suppression of nuclear factor kappa B (NF-κB)-mediated inflammatory pathway. Male Sprague–Dawley rats were treated with vehicle or metformin (50 mg/kg daily, i.p.) for 3 weeks and were subjected to permanent middle cerebral artery occlusion (pMCAO). At 24 h (acute phase) and 96 h (subacute phase) after pMCAO, infarct volume and neurological deficits were evaluated. Meanwhile, the activity of NF-κB and the levels of its downstream pro-inflammatory cytokines were detected at 24 h after pMCAO. Our results...
Source: Molecular Neurobiology - July 21, 2015 Category: Neurology Source Type: research
Protocatechualdehyde Protects Against Cerebral Ischemia-Reperfusion-Induced Oxidative Injury Via Protein Kinase Cε/Nrf2/HO-1 Pathway
Abstract
Oxidative stress is closely related to the pathogenesis of ischemic stroke. Protocatechualdehyde (PCA) is a phenolic acid compound that has the putative antioxidant activities. The present study was aimed to investigate the molecular mechanisms involved in the antioxidative effect of PCA against cerebral ischemia/reperfusion (I/R) injury. The experiment stroke model was produced in Sprague–Dawley rats via middle cerebral artery occlusion (MCAO). To model ischemia-like conditions in vitro, differentiated SH-SY5Y cells were exposed to transient oxygen and glucose deprivation (OGD). Treatment with PCA sign...
Source: Molecular Neurobiology - January 16, 2016 Category: Neurology Source Type: research
Conditioned Medium Derived from Neural Progenitor Cells Induces Long-term Post-ischemic Neuroprotection, Sustained Neurological Recovery, Neurogenesis, and Angiogenesis
Abstract
Adult neural progenitor cells (NPCs) induce post-ischemic long-term neuroprotection and brain remodeling by releasing of survival- and plasticity-promoting mediators. To evaluate whether secreted factors may mimic neuroprotective and restorative effects of NPCs, we exposed male C57BL6 mice to focal cerebral ischemia and intravenously applied conditioned medium (CM) derived from subventricular zone NPCs. CM dose-dependently reduced infarct volume and brain leukocyte infiltration after 48 h when delivered up to 12 h after focal cerebral ischemia. Neuroprotection persisted in the post-acute stroke phase yi...
Source: Molecular Neurobiology - February 9, 2016 Category: Neurology Source Type: research
High Plasma Levels of d -Dimer Are Independently Associated with a Heightened Risk of Deep Vein Thrombosis in Patients with Intracerebral Hemorrhage
AbstractDeep venous thrombosis (DVT) is a complication of stroke. Our aim was to determine whetherd-dimer plasma levels at admission could be a risk factor for DVT in Chinese patients with acute intracerebral hemorrhage (ICH). From December 2012 to November 2014, all patients with first-ever acute ICH were included. At baseline, the demographical and clinical data were taken. These patients were assessed for DVT using color Doppler ultrasonography (CDUS) on 15 days after ICH and whenever clinically requested. Multivariate analyses were performed using logistic regression models. Receiver operating characteristic (ROC) cu...
Source: Molecular Neurobiology - September 6, 2016 Category: Neurology Source Type: research
MiR-181b Antagonizes Atherosclerotic Plaque Vulnerability Through Modulating Macrophage Polarization by Directly Targeting Notch1
AbstractAtherosclerotic plaque vulnerability is the major cause for acute stroke and could be regulated by macrophage polarization. MicroRNA-181b (miR-181b) was involved in macrophage differential. Here, we explore whether miR-181b could regulate atherosclerotic plaque vulnerability by modulating macrophage polarization and the underline mechanisms. In acute stroke patients with atherosclerotic plaque, we found that the serum level of miR-181b was decreased. Eight-week apolipoprotein E knockout (ApoE−/−) mice were randomly divided into three groups (N = 10): mice fed with normal saline (Ctrl), mice fed with high-fat ...
Source: Molecular Neurobiology - October 7, 2016 Category: Neurology Source Type: research
Protein Profile and Morphological Alterations in Penumbra after Focal Photothrombotic Infarction in the Rat Cerebral Cortex
AbstractAfter ischemic stroke, cell damage propagates from infarct core to surrounding tissues (penumbra). To reveal proteins involved in neurodegeneration and neuroprotection in penumbra, we studied protein expression changes in 2-mm ring around the core of photothrombotic infarct induced in the rat brain cortex by local laser irradiation after administration of Bengal Rose. The ultrastructural study showed edema and degeneration of neurons, glia, and capillaries. Morphological changes gradually decreased across the penumbra. Using the antibody microarrays, we studied changes in expression of>200 neuronal proteins in p...
Source: Molecular Neurobiology - July 13, 2017 Category: Neurology Source Type: research
Inhibition of Peroxynitrite-Induced Mitophagy Activation Attenuates Cerebral Ischemia-Reperfusion Injury
AbstractActivated autophagy/mitophagy has been intensively observed in ischemic brain, but its roles remain controversial. Peroxynitrite (ONOO−), as a representative of reactive nitrogen species, is considered as a critical neurotoxic factor in mediating cerebral ischemia-reperfusion (I/R) injury, but its roles in autophagy/mitophagy activation remain unclear. Herein, we hypothesized that ONOO− could induce PINK1/Parkin-mediated mitophagy activation via triggering dynamin-related protein 1 (Drp1) recruitment to damaged mitochondria, contributing to cerebral I/R injury. Firstly, we found PINK1/Parkin-mediated mitophagy ...
Source: Molecular Neurobiology - January 6, 2018 Category: Neurology Source Type: research
Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication
AbstractNeurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e.g., Alzheimer ’s disease), have always been one of the leading cause of morbidity and mortality worldwide. These debilitating diseases represent an enormous disease burden, not only in terms of health suffering but also in economic costs. Although the clinical presentations differ for these diseases, a growing body of evidence suggests that oxidative stress and inflammatory responses in brain tissue significantly contribute to their pathology. However, therapies attempting to prevent oxidative damage o...
Source: Molecular Neurobiology - February 27, 2018 Category: Neurology Source Type: research
Genetic Deletion of Kr üppel-Like Factor 11 Aggravates Ischemic Brain Injury
AbstractKr üppel-like factors (KLFs) belong to the zinc finger family of transcription factors, and their function in the CNS is largely unexplored. KLF11 is a member of the KLF family, and we have previously demonstrated that peroxisome proliferator-activated receptor gamma-mediated cerebral protection durin g ischemic insults needs recruitment of KLF11 as its critical coactivator. Here, we sought to determine the role of KLF11 itself in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion (MCAO) was performed in KLF11 knockout and wild-type contro l mice, and brain...
Source: Molecular Neurobiology - March 8, 2018 Category: Neurology Source Type: research
