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Source: Metabolic Brain Disease
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Total 151 results found since Jan 2013.
Long non-coding RNA SNHG7 upregulates FGF9 to alleviate oxygen and glucose deprivation-induced neuron cell injury in a miR-134-5p-dependent manner
AbstractLong non-coding RNA small nucleolar RNA host gene 7 (SNHG7) was reported to regulate the pathogenesis of ischemic stroke. The study aimed to disclose SNHG7 role in oxygen and glucose deprivation (OGD)-induced Neuro-2a (N2a) cell disorders. An OGD injury cell model was established using N2a cells. The expression of SNHG7, microRNA-134-5p (miR-134-5p) and fibroblast growth factor 9 (FGF9) was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by western blot. Cell viability and Lactate Dehydrogenase (LDH) leakage were determined by cell counting kit-8 and LDH activity dete...
Source: Metabolic Brain Disease - October 18, 2021 Category: Neurology Source Type: research
Neuroprotective effect of herniarin following transient focal cerebral ischemia in rats
AbstractIschemic stroke is a devastating central nervous disease. Despite extensive research in to this area, few innovative neuroprotective treatments have been presented. 7-methoxycoumarin, also known as herniarin, is a common natural coumarin in several plant species. This project examined the effects of the herniarin in rats subjected to the middle cerebral artery occlusion (MCAO). Herniarin at doses of 10 and 20 mg/kg was administered through intraperitoneal injection for 7 days before MCAO induction. Rats were subjected to a 30 min MCAO and a subsequent 24 h’ reperfusion. 24 h after the termination of MCAO, n...
Source: Metabolic Brain Disease - November 11, 2021 Category: Neurology Source Type: research
Stellate ganglion block suppresses hippocampal ferroptosis to attenuate cerebral ischemia-reperfusion injury via the Hippo pathway
In conclusion, SGB inhibited ferroptosis of hippocampal neurons via activating the Hippo pathway and thereby alleviated I/R injury. The data provide a novel insight into the treatment of ischemic stroke and even other ischemic encephalopathies.Graphical Abstract
Source: Metabolic Brain Disease - March 16, 2023 Category: Neurology Source Type: research
Erratum to: A novel HLA-DRα1-MOG-35-55 construct treats experimental stroke
Source: Metabolic Brain Disease - September 1, 2014 Category: Neurology Source Type: research
Pannexin1 as a novel cerebral target in pathogenesis of hepatic encephalopathy
Abstract
Hepatic encephalopathy (HE) represents a nervous system disorder caused due to liver dysfunction. HE is broadly classified as acute/overt and moderate-minimal HE. Since HE syndrome severely affects quality of life of the patients and it may be life threatening, it is important to develop effective therapeutic strategy against HE. Mainly ammonia neurotoxicity is considered accountable for HE. Increased level of ammonia in the brain activates glutamate-NMDA (N-methyl-D-aspartate) receptor (NMDAR) pathway leading to Ca2+ influx, energy deficit and oxidative stress in the post synaptic neurons. Moreover, NMD...
Source: Metabolic Brain Disease - November 20, 2014 Category: Neurology Source Type: research
Erratum to: Tumor necrosis factor beta Nco I polymorphism (rs909253) is associated with inflammatory and metabolic markers in acute ischemic stroke
Source: Metabolic Brain Disease - January 15, 2015 Category: Neurology Source Type: research
Near infrared radiation rescues mitochondrial dysfunction in cortical neurons after oxygen-glucose deprivation
In this study, we tested the hypothesis that low intensity NIR may attenuate hypoxia/ischemia-induced mitochondrial dysfunction in neurons. Primary cortical mouse neuronal cultures were subjected to 4 h oxygen-glucose deprivation followed by reoxygenation for 2 h, neurons were then treated with a 2 min exposure to 810-nm NIR. Mitochondrial function markers including MTT reduction and mitochondria membrane potential were measured at 2 h after treatment. Neurotoxicity was quantified 20 h later. Our results showed that 4 h oxygen-glucose deprivation plus 20 h reoxygenation caused 33.8 ± 3.4 % of neuron death, whi...
Source: Metabolic Brain Disease - March 6, 2015 Category: Neurology Source Type: research
Inherited neurovascular diseases affecting cerebral blood vessels and smooth muscle
Abstract
Neurovascular diseases are among the leading causes of mortality and permanent disability due to stroke, aneurysm, and other cardiovascular complications. Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and Marfan syndrome are two neurovascular disorders that affect smooth muscle cells through accumulation of granule and osmiophilic materials and defective elastic fiber formations respectively. Moyamoya disease, hereditary hemorrhagic telangiectasia (HHT), microcephalic osteodysplastic primordial dwarfism type II (MOPD II), and Fabry’s disease are dis...
Source: Metabolic Brain Disease - April 21, 2015 Category: Neurology Source Type: research
Near infrared radiation protects against oxygen-glucose deprivation-induced neurotoxicity by down-regulating neuronal nitric oxide synthase (nNOS) activity in vitro
Abstract
Near infrared radiation (NIR) has been shown to be neuroprotective against neurological diseases including stroke and brain trauma, but the underlying mechanisms remain poorly understood. In the current study we aimed to investigate the hypothesis that NIR may protect neurons by attenuating oxygen-glucose deprivation (OGD)-induced nitric oxide (NO) production and modulating cell survival/death signaling. Primary mouse cortical neurons were subjected to 4 h OGD and NIR was applied at 2 h reoxygenation. OGD significantly increased NO level in primary neurons compared to normal control, which was signific...
Source: Metabolic Brain Disease - April 29, 2015 Category: Neurology Source Type: research
Metformin improves anxiety-like behaviors through AMPK-dependent regulation of autophagy following transient forebrain ischemia
Abstract
Stroke is one of the main threats to the public health worldwide. Metformin, an anti-diabetic drug, is an activator of AMP-activated protein kinase (AMPK). Metformin plays an important role on improving behavior in neurodegenerative diseases through diverse pathways. In the current study we aimed to investigate the probable effects of metformin on anxiety and autophagy pathway in global cerebral ischemia. Rats were divided into seven groups; Sham, ischemia (I/R), metformin (met), compound c (CC), CC+ischemia, met+ischemia, met+CC+ischemia. Metformin was pretreated for 2 weeks and CC administrated half a...
Source: Metabolic Brain Disease - September 5, 2015 Category: Neurology Source Type: research
Neuron specific enolase: a promising therapeutic target in acute spinal cord injury
Abstract
Enolase is a multifunctional protein, which is expressed abundantly in the cytosol. Upon stimulatory signals, enolase can traffic to cell surface and contribute to different pathologies including injury, autoimmunity, infection, inflammation, and cancer. Cell-surface expression of enolase is often detected on activated macrophages, microglia/macrophages, microglia, and astrocytes, promoting extracellular matrix degradation, production of pro-inflammatory cytokines/chemokines, and invasion of inflammatory cells in the sites of injury and inflammation. Inflammatory stimulation also induces translocation of ...
Source: Metabolic Brain Disease - February 5, 2016 Category: Neurology Source Type: research
Retinoic acid-pretreated Wharton ’s jelly mesenchymal stem cells in combination with triiodothyronine improve expression of neurotrophic factors in the subventricular zone of the rat ischemic brain injury
In conclusion, application of RA-pretreated WJ-MSCs + T3 could be beneficial in exerting better neurotrophic function probably via modulation of pro-inflammatory cytokines.
Source: Metabolic Brain Disease - August 21, 2016 Category: Neurology Source Type: research
