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Source: Neurochemical Research

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Total 300 results found since Jan 2013.

Liraglutide Ameliorates Cerebral Ischemia in Mice via Antipyroptotic Pathways
In this study, we found that injection of Lg significantly improved the recovery of motor function, increased cerebral blood flow and ameliorated cerebral damage in a mouse model of focal cerebral cortical ischemia. Our results revealed that Lg treatment significantly reduced the levels of NLRP3, Caspase1, IL-1β and the pore-forming protein gasdermin D in microglial cells in vitro, suggesting that the neuroprotective effect of Lg may be achieved through the inhibition of pyroptosis. Furthermore, by using a specific inhibitor of NOD-like receptor protein 3 (NLRP3), we confirmed that the antipyroptotic mechanism of Lg may b...
Source: Neurochemical Research - March 30, 2022 Category: Neuroscience Authors: Lan Yang Junmin Cheng Guang Shi Cong Zhang Yuanyuan Du Linyu Chen Huimin Qiao Rong Chen Xiangjian Zhang Source Type: research

Panax notoginseng Saponins Protect Brain Microvascular Endothelial Cells against Oxygen-Glucose Deprivation/Resupply-Induced Necroptosis via Suppression of RIP1-RIP3-MLKL Signaling Pathway
This study provided a novel insight of PNS application in clinics.PMID:35904697 | DOI:10.1007/s11064-022-03675-0
Source: Neurochemical Research - July 29, 2022 Category: Neuroscience Authors: Yanhong Hu Hongtao Lei Sai Zhang Jiabao Ma Soyeon Kang Liangqin Wan Fanghe Li Fan Zhang Tianshi Sun Chujun Zhang Weihong Li Source Type: research

Cell Death Mechanisms in Cerebral Ischemia-Reperfusion Injury
Neurochem Res. 2022 Aug 17. doi: 10.1007/s11064-022-03697-8. Online ahead of print.ABSTRACTIschemic stroke is one of the major causes of morbidity and mortality, affecting millions of people worldwide. Inevitably, the interruption of cerebral blood supply after ischemia may promote a cascade of pathophysiological processes. Moreover, the subsequent restoration of blood flow and reoxygenation may further aggravate brain tissue injury. Although recombinant tissue plasminogen activator (rt-PA) is the only approved therapy for restoring blood perfusion, the reperfusion injury and the narrow therapeutic time window restrict its...
Source: Neurochemical Research - August 17, 2022 Category: Neuroscience Authors: Qian Zhang Meng Jia YunFu Wang Qun Wang Jianping Wu Source Type: research

Vitexin Improves Cerebral ischemia ‑reperfusion Injury by Attenuating Oxidative Injury and Ferroptosis via Keap1/Nrf2/HO-1signaling
In this study, we established the oxygen-glucose deprivation and reoxygenation (OGD/R) neuron cell and middle cerebral artery occlusion/reperfusion (MCAO/R) rat model. The cell viability, cell apoptosis and reactive oxygen species (ROS) levels were tested by CCK-8 assay and Flow cytometry, respectively. Hematoxylin-eosin staining, TTC, TEM, immunofluorescence analysis and western blot were used to investigate the effects of Vitexin. The results demonstrated that Vitexin could enhanced the cell viability and decreased the cell apoptosis in OGD/R cell model. Meanwhile, incubation with Vitexin maintained the neuroprotective e...
Source: Neurochemical Research - November 26, 2022 Category: Neuroscience Authors: Lei Guo Lei Shi Source Type: research

Reduced beta-catenin expression in the hippocampal CA1 region following transient cerebral ischemia in the gerbil.
In this study, we examined changes of expression in beta-catenin in the hippocampal CA1 region of the gerbil following 5 min of transient cerebral ischemia. We observed neuronal damage using cresyl violet staining, neuronal nuclei immunohistochemistry and Fluro-Jade B immunofluorescence. Four days after ischemia-reperfusion (I-R), most of pyramidal cells in the CA1 region were damaged. In addition, early damage in dendrites was detected 1 day after I-R by immunohistochemical staining for microtubule-associated protein 2 (MAP-2), and MAP-2 immunoreactivity was hardly detected in the CA1 region 4 days after I-R. We found tha...
Source: Neurochemical Research - May 1, 2013 Category: Neuroscience Authors: Cho JH, Yan BC, Lee YJ, Park JH, Ahn JH, Kim IH, Lee JC, Kim YM, Lee B, Cho JH, Won MH Tags: Neurochem Res Source Type: research

Intracellular Ion Channel CLIC1: Involvement in Microglia-Mediated β-Amyloid Peptide(1-42) Neurotoxicity.
Abstract Microglia can exacerbate central nervous system disorders, including stroke and chronic progressive neurodegenerative diseases such as Alzheimer disease. Mounting evidence points to ion channels expressed by microglia as contributing to these neuropathologies. The Chloride Intracellular Channel (CLIC) family represents a class of chloride intracellular channel proteins, most of which are localized to intracellular membranes. CLICs are unusual in that they possess both soluble and integral membrane forms. Amyloid β-peptide (Aβ) accumulation in plaques is a hallmark of familial Alzheimer disease. The trun...
Source: Neurochemical Research - June 7, 2013 Category: Neuroscience Authors: Skaper SD, Facci L, Giusti P Tags: Neurochem Res Source Type: research

Neuroprotective Evaluation of Tilia americana and Annona diversifolia in the Neuronal Damage Induced by Intestinal Ischemia.
This study was conducted to test aqueous and organic extracts of these two plants for neuroprotective effects in a novel experimental model of intestinal ischemia in situ. T. americana and A. diversifolia aqueous and organic extracts were administrated to guinea pigs at an oral dose of 100 and 300 mg/kg for 15 days. Twenty four hours after the last administration, the animals were anesthetized and intestinal ischemia in situ was induced by clamping for 80 min selected branches of the superior mesenteric artery. Ischemic segments placed in an in vitro organ bath were stimulated electrically (0.3 Hz frequency, 3.0 ms du...
Source: Neurochemical Research - June 6, 2013 Category: Neuroscience Authors: Angeles-López GE, González-Trujano ME, Déciga-Campos M, Ventura-Martínez R Tags: Neurochem Res Source Type: research

Changes in Levels of Hypoxia-Induced Mediators in Rat Hippocampus During Chronic Cerebral Hypoperfusion.
Abstract The hypoxia-inducible factor (HIF)-mediated signaling pathway is an adaptive and protective mechanism that is triggered by hypoxia, ischemia, and other pathophysiological conditions. The expression of HIF-1α and downstream genes, some of which are pro-apoptotic whereas others are pro-survival, is up-regulated in ischemic stroke. Interestingly, however, the effects of HIF-1α activation are different in the early and late stages of acute cerebral ischemia, and these differences may depend on the duration and severity of hypoxia. Therefore, in the present study, we investigated the effect of HIF-1α activa...
Source: Neurochemical Research - September 26, 2013 Category: Neuroscience Authors: Yang Y, Zhang J, Liu H, Wang J, Xin J, Deng M Tags: Neurochem Res Source Type: research

XQ-1H Suppresses Neutrophils Infiltration and Oxidative Stress Induced by Cerebral Ischemia Injury Both In Vivo and In Vitro.
In this study, we investigated the anti-inflammatory and anti-oxidative activities of XQ-1H in vivo and vitro. In our study, rats were treating with XQ-1H (31.2, 15.6 and 7.8 mg/kg) after middle cerebral artery occlusion surgery. Primary cultured cortical rat neurons were treated with Na2S2O4 for 1.5 h to mimic hypoxia and reoxygenation injury in vitro. Cortical neurons were preincubated with XQ-1H (100, 10, 1 μM) 24 h before hypoxic injury. Brain edema was evaluated by brain water content. Neutrophil infiltration was determined by fluorescence imaging method and myeloperoxidase assay. Intercellular adhesion molecule ...
Source: Neurochemical Research - October 12, 2013 Category: Neuroscience Authors: Wei J, Fang W, Sha L, Han D, Zhang R, Hao X, Li Y Tags: Neurochem Res Source Type: research

A Novel Prolyl Hydroxylase Inhibitor Protects Against Cell Death After Hypoxia.
In this study, we investigated how TM6008 affects cell survival after hypoxic conditions capable of inducing HIF-1α expression and how TM6008 regulates PHDs and genes downstream of HIF-1α. After SHSY-5Y cells had been subjected to hypoxia, TM6008 was added to the cell culture medium under normoxic conditions. Apoptotic cell death was significantly augmented just after the hypoxic conditions, compared with cell death under normoxic conditions. Notably, when TM6008 was added to the media after the cells had been subjected to hypoxia, the expression level of HIF-1α increased and the number of cell deaths decreased, compare...
Source: Neurochemical Research - October 17, 2013 Category: Neuroscience Authors: Kontani S, Nagata E, Uesugi T, Moriya Y, Fujii N, Miyata T, Takizawa S Tags: Neurochem Res Source Type: research

Effects of Amide Creatine Derivatives in Brain Hippocampal Slices, and Their Possible Usefulness for Curing Creatine Transporter Deficiency.
Abstract The creatine/phosphocreatine system carries ATP from production to consumption sites and buffers the intracellular content of ATP at times of energy deprivation. The creatine transporter deficiency syndrome is an X-linked disease caused by a defective creatine transporter into the central nervous system. This disease is presently untreatable because creatine lacking its carrier cannot cross neither the blood-brain barrier nor the cell plasma membranes. Possible strategies to cure this condition are to couple creatine to molecules which have their own carrier, to exploit the latter to cross biological memb...
Source: Neurochemical Research - November 12, 2013 Category: Neuroscience Authors: Garbati P, Adriano E, Salis A, Ravera S, Damonte G, Millo E, Balestrino M Tags: Neurochem Res Source Type: research