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Source: Neurochemical Research

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Total 300 results found since Jan 2013.

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro.
Abstract The products of elastin degradation, namely elastin-derived peptides (EDPs), are detectable in the cerebrospinal fluid of healthy individuals and in patients after ischemic stroke, and their number increases with age. Depending on their concentrations, both nitric oxide (NO) and reactive oxygen species (ROS) take part either in myocardial ischemia reperfusion injury or in neurovascular protection after ischemic stroke. The aim of our study was to determine the impact of VGVAPG peptide on ROS and NO production and expression of endothelial nitric oxide synthase (eNos), inducible nitric oxide synthase (iNos...
Source: Neurochemical Research - February 13, 2019 Category: Neuroscience Authors: Szychowski KA, Gmiński J Tags: Neurochem Res Source Type: research

Inhibition of Calcium/Calmodulin-Dependent Protein Kinase II α Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase.
Inhibition of Calcium/Calmodulin-Dependent Protein Kinase IIα Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase. Neurochem Res. 2019 Mar 27;: Authors: Wei Y, Wang R, Teng J Abstract Ischemic stroke is a leading cause of mortality and morbidity worldwide, and oxidative stress plays a significant role in the ischemia stage and reperfusion stage. Previous studies have indicated that both calcium/calmodulin-dependent protein kinase II (CaMKII) and glucose 6-phosphate dehydrogenase (G6PD) are involved in the oxidative stress. Thus, the aim of this st...
Source: Neurochemical Research - March 26, 2019 Category: Neuroscience Authors: Wei Y, Wang R, Teng J Tags: Neurochem Res Source Type: research

TGF- β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats.
TGF-β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats. Neurochem Res. 2019 Sep 25;: Authors: Peng L, Yin J, Wang S, Ge M, Han Z, Wang Y, Zhang M, Xie L, Li Y Abstract Evidence has shown the therapeutic potential of isoflurane (ISO) in cerebral stroke. The present study investigated the mechanism of ISO on vascular endothelial growth factor (VEGF) and CD34 expression in a rat model of stroke. Transient focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) for 1 ...
Source: Neurochemical Research - September 24, 2019 Category: Neuroscience Authors: Peng L, Yin J, Wang S, Ge M, Han Z, Wang Y, Zhang M, Xie L, Li Y Tags: Neurochem Res Source Type: research

miR-124-5p/NOX2 Axis Modulates the ROS Production and the Inflammatory Microenvironment to Protect Against the Cerebral I/R Injury.
In conclusion, miR-124-5p/NOX2 axis modulates NOX-mediated ROS production, the inflammatory microenvironment, subsequently the apoptosis of neurons, finally affecting the cerebral I/R injury. PMID: 31950451 [PubMed - as supplied by publisher]
Source: Neurochemical Research - January 15, 2020 Category: Neuroscience Authors: Wu Y, Yao J, Feng K Tags: Neurochem Res Source Type: research

Attenuation of Acute Intracerebral Hemorrhage-Induced Microglial Activation and Neuronal Death Mediated by the Blockade of Metabotropic Glutamate Receptor 5 In Vivo.
In this study, collagenase-induced ICH mice received a single intraperitoneal injection of the mGluR5 antagonist-, MTEP, or vehicle 2 h after injury. We found that acute ICH upregulated mGluR5 and microglial activation. mGluR5 was highly localized in reactive microglia in the peri-hematomal cortex and striatum on days 3 and 7 post-ICH. The MTEP-mediated pharmacological inhibition of mGluR5 in vivo resulted in the substantial attenuation of acute microglial activation and IL-6, and TNF-α release. We also showed that the blockade of mGluR5 markedly reduced cell apoptosis, and neurodegeneration and markedly elevated neuropr...
Source: Neurochemical Research - March 4, 2020 Category: Neuroscience Authors: Rahman MS, Yang J, Luan Y, Qiu Z, Zhang J, Lu H, Chen X, Liu Y Tags: Neurochem Res Source Type: research

A Critical Role for ISGylation, Ubiquitination and, SUMOylation in Brain Damage: Implications for Neuroprotection.
Abstract Post-translational modification (PTMs) of proteins by ubiquitin and ubiquitin-like modifiers such as interferon-stimulated gene 15 (ISG15) and small ubiquitin-related modifier (SUMO) play a critical role in the regulation of brain pathophysiology. Protein ISGylation is a covalent attachment of ISG15 to its target proteins, which is a unique PTM among other ubiquitin-like modifiers. Although, ISG15 shares sequence homology to ubiquitin, yet the functional significance of protein ISGylation is distinct from ubiquitination and SUMOylation. Further, ISG15 highly conserved among vertebrate species, unlike the ...
Source: Neurochemical Research - June 3, 2020 Category: Neuroscience Authors: Nakka VP, Mohammed AQ Tags: Neurochem Res Source Type: research

Guanosine Neuroprotective Action in Hippocampal Slices Subjected to Oxygen and Glucose Deprivation Restores ATP Levels, Lactate Release and Glutamate Uptake Impairment: Involvement of Nitric Oxide.
This study was designed to investigate the involvement of nitric oxide (NO) in the mechanisms related to the protective role of guanosine in rat hippocampal slices subjected to OGD followed by reoxygenation (OGD/R). Guanosine (100 μM) and the pan-NOS inhibitor, L-NAME (1 mM) afforded protection to hippocampal slices subjected to OGD/R. The presence of NO donors, DETA-NO (800 μM) or SNP (5 μM) increased reactive species production, and abolished the protective effect of guanosine or L-NAME against OGD/R. Guanosine or L-NAME treatment prevented the impaired ATP production, lactate release, and glutamate uptake followi...
Source: Neurochemical Research - July 13, 2020 Category: Neuroscience Authors: Thomaz DT, Andreguetti RR, Binder LB, Scheffer DDL, Corrêa AW, Silva FRMB, Tasca CI Tags: Neurochem Res Source Type: research

Hyperbaric Oxygen Preconditioning Protects Against Cerebral Ischemia/Reperfusion Injury by Inhibiting Mitochondrial Apoptosis and Energy Metabolism Disturbance.
Abstract Hyperbaric oxygen (HBO) therapy is considered a safe and feasible method that to provide neuroprotection against ischemic stroke. However, the therapy mechanisms of HBO have not been fully elucidated. We hypothesized that the mechanism underlying the protective effect of HBO preconditioning (HBO-PC) against cerebral ischemia/reperfusion injury was related to inhibition of mitochondrial apoptosis and energy metabolism disorder. To test this hypothesis, an ischemic stroke model was established by middle cerebral artery occlusion (MCAO) in rats. HBO-PC involved five consecutive days of pretreatment before MC...
Source: Neurochemical Research - January 16, 2021 Category: Neuroscience Authors: Wang SD, Fu YY, Han XY, Yong ZJ, Li Q, Hu Z, Liu ZG Tags: Neurochem Res Source Type: research

Comparative Assessment of the Proteolytic Stability and Impact of Poly-Arginine Peptides R18 and R18D on Infarct Growth and Penumbral Tissue Preservation Following Middle Cerebral Artery Occlusion in the Sprague Dawley Rat.
Abstract Poly-arginine peptides R18 and R18D have previously been demonstrated to be neuroprotective in ischaemic stroke models. Here we examined the proteolytic stability and efficacy of R18 and R18D in reducing infarct core growth and preserving the ischaemic penumbra following middle cerebral artery occlusion (MCAO) in the Sprague Dawley rat. R18 (300 or 1000 nmol/kg), R18D (300 nmol/kg) or saline were administered intravenously 10 min after MCAO induced using a filament. Serial perfusion and diffusion-weighted MRI imaging was performed to measure changes in the infarct core and penumbra from time points bet...
Source: Neurochemical Research - February 1, 2021 Category: Neuroscience Authors: Milani D, Clark VW, Feindel KW, Blacker DJ, Bynevelt M, Edwards AB, Anderton RS, Knuckey NW, Meloni BP Tags: Neurochem Res Source Type: research

Spata2 Knockdown Exacerbates Brain Inflammation via NF- κB/P38MAPK Signaling and NLRP3 Inflammasome Activation in Cerebral Ischemia/Reperfusion Rats
Neurochem Res. 2021 Jun 1. doi: 10.1007/s11064-021-03360-8. Online ahead of print.ABSTRACTBrain inflammation induced by ischemic stroke is an important cause of secondary brain injury. The nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and NLRP3 inflammasome signaling are believed to drive the progression of brain inflammation. Spermatogenesis-associated protein2 (SPATA2) functions as a partner protein that recruits CYLD, a negative regulator of NF-κB signaling, to signaling complexes. However, the role of SPATA2 in the central nervous system remains unclear and whether it is involved in regulat...
Source: Neurochemical Research - June 2, 2021 Category: Neuroscience Authors: Yikun Ren Jin Jiang Wenxia Jiang Xueling Zhou Wenhao Lu Jingwen Wang Yong Luo Source Type: research

Medicarpin Protects Cerebral Microvascular Endothelial Cells Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury via the PI3K/Akt/FoxO Pathway: A Study of Network Pharmacology Analysis and Experimental Validation
In conclusion, medicarpin suppressed OGD/R-induced injury in HCMECs by activating PI3K/Akt/FoxO pathway.PMID:34523056 | DOI:10.1007/s11064-021-03449-0
Source: Neurochemical Research - September 15, 2021 Category: Neuroscience Authors: Yu Wang Ronggang Yang Feng Yan Yeqiang Jin Xu Liu Tiancai Wang Source Type: research