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Total 79 results found since Jan 2013.

Cerebellar Fastigial Nucleus Stimulation in a Chronic Unpredictable Mild Stress Rat Model Reduces Post-Stroke Depression by Suppressing Brain Inflammation via the microRNA-29c/TNFRSF1A Signaling Pathway.
CONCLUSIONS In a rat model, cerebellar fastigial nucleus stimulation reduced the expression of TNFRSF1A by upregulating miR-29c expression, which suppressed the expression of inflammatory cytokines, resulting in reduced severity of post-stroke depression. PMID: 31352465 [PubMed - in process]
Source: Medical Science Monitor - July 30, 2019 Category: Research Tags: Med Sci Monit Source Type: research

Fibrinogen nitrotyrosination after ischemic stroke impairs thrombolysis and promotes neuronal death.
lanas A, Roquer J, Valverde MA, Muñoz FJ Abstract Ischemic stroke is an acute vascular event that compromises neuronal viability, and identification of the pathophysiological mechanisms is critical for its correct management. Ischemia produces increased nitric oxide synthesis to recover blood flow but also induces a free radical burst. Nitric oxide and superoxide anion react to generate peroxynitrite that nitrates tyrosines. We found that fibrinogen nitrotyrosination was detected in plasma after the initiation of ischemic stroke in human patients. Electron microscopy and protein intrinsic fluorescence showed that...
Source: Biochimica et Biophysica Acta - December 12, 2014 Category: Biochemistry Authors: Ill-Raga G, Palomer E, Ramos-Fernández E, Guix FX, Bosch-Morató M, Guivernau B, Tajes M, Valls-Comamala V, Jiménez-Conde J, Ois A, Pérez-Asensio F, Reyes-Navarro M, Caballo C, Gil-Gómez G, López-Vílchez I, Galán AM, Alameda F, Escolar G, Opazo C, Tags: Biochim Biophys Acta Source Type: research

Fibrinogen nitrotyrosination after ischemic stroke impairs thrombolysis and promotes neuronal death
Publication date: Available online 12 December 2014 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Author(s): Gerard ILL-Raga , Ernest Palomer , Eva Ramos-Fernández , Francesc X. Guix , Mònica Bosch-Morató , Biuse Guivernau , Marta Tajes , Victòria Valls-Comamala , Jordi Jiménez-Conde , Angel Ois , Fernando Pérez-Asensio , Mario Reyes-Navarro , Carolina Caballo , Gabriel Gil-Gómez , Irene López-Vílchez , Ana M. Galán , Francesc Alameda , Ginés Escolar , Carlos Opazo , Anna Planas , Jaume Roquer , Miguel A. Valverde , Francisco J. Muñoz Ischemic stroke is an acute vascular event that c...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - December 25, 2014 Category: Molecular Biology Source Type: research

Neurotrophic and neuroprotective effects of oxyntomodulin in neuronal cells and a rat model of stroke.
In this study, the neuroprotective effect of OXM was first examined in human neuroblastoma (SH-SY5Y) cells and rat primary cortical neurons. GLP-1R and GCGR antagonists, and inhibitors of various signaling pathways were used in cell culture to characterize the mechanisms of action of OXM. To evaluate translation in vivo, OXM-mediated neuroprotection was assessed in a 60-min, transient middle cerebral artery occlusion (MCAo) rat model of stroke. We found that OXM dose- and time-dependently increased cell viability and protected cells from glutamate toxicity and oxidative stress. These neuroprotective actions of OXM were mai...
Source: Experimental Neurology - November 13, 2016 Category: Neurology Authors: Li Y, Wu KJ, Yu SJ, Tamargo IA, Wang Y, Greig NH Tags: Exp Neurol Source Type: research

Up-regulation of miR-122 protects against neuronal cell death in ischemic stroke through the heat shock protein 70-dependent NF- κB pathway by targeting FOXO3.
Up-regulation of miR-122 protects against neuronal cell death in ischemic stroke through the heat shock protein 70-dependent NF-κB pathway by targeting FOXO3. Exp Cell Res. 2018 Apr 28;: Authors: Guo D, Ma J, Li T, Yan L Abstract Dysfunction of the microRNA (miR) network has been emerging as a main regulator in ischemic stroke. Recently, studies have linked the deregulation of miR-122 to ischemic stroke. However, the specific role and molecular mechanism of miR-122 in ischemic stroke remain to be further investigated. Here, we found that miR-122 was decreased in mouse N2A neuroblastoma (N2A) cells af...
Source: Experimental Cell Research - April 28, 2018 Category: Cytology Authors: Guo D, Ma J, Li T, Yan L Tags: Exp Cell Res Source Type: research

Early Transplantation of Human Cranial Bone-derived Mesenchymal Stem Cells Enhances Functional Recovery in Ischemic Stroke Model Rats.
Authors: Oshita J, Okazaki T, Mitsuhara T, Imura T, Nakagawa K, Otsuka T, Kurose T, Tamura T, Abiko M, Takeda M, Kawahara Y, Yuge L, Kurisu K Abstract We analyzed the cell characteristics, neuroprotective, and transplantation effects of human cranial bone-derived mesenchymal stem cells (hcMSCs) in ischemic stroke model rats compared with human iliac bone-derived mesenchymal stem cells (hiMSCs). The expressions of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF ) as neurotrophic factors were analyzed in both MSCs. hiMSCs or hcMSCs were intravenously administered into ischemic st...
Source: Neurologia Medico-Chirurgica - January 22, 2020 Category: Neurosurgery Tags: Neurol Med Chir (Tokyo) Source Type: research

Neuroprotective effects of miR-532-5p against ischemic stroke
In this study, we established anin vivo middle cerebral artery occlusion (MCAO) model in mice. The expression level of miR-532-5p, neurological score, infarct area, neuronal apoptosis, and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway-related molecules were examined. Low miR-532-5p levels and high phosphatase and tensin homolog deleted on chromosome 10 (PTEN) levels were detected in the mouse MCAO model. MiR-532-5p overexpression improved neurological dysfunction, reduced the infarct area, attenuated neuronal injury and apoptosis, and promoted the activation of the PI3K/Akt signaling pathway in MCAO mice. In vitro...
Source: Metabolic Brain Disease - February 20, 2020 Category: Neurology Source Type: research

Increase of Cry 1 expression is a common phenomenon of the disturbed circadian clock in ischemic stroke and opioid addiction
Biochem Biophys Res Commun. 2021 Apr 21;558:8-13. doi: 10.1016/j.bbrc.2021.04.053. Online ahead of print.ABSTRACTIncreasing evidences suggest the involvement of disrupted circadian clock in various pathologies including stroke and substance abuse. Here we took an attempt to do a comparative study on the regulation of circadian clock gene expression under two pathological circumstances - Opioid addiction and Ischemic stroke in the same cell line model (human neuroblastoma SH-SY5Y cells). To mimic in vivo ischemic stroke condition cells were placed in a hypoxia chamber and incubated for 10 h in balanced salt solution lacking...
Source: Biochemical and Biophysical Research communications - April 24, 2021 Category: Biochemistry Authors: Kaninika Roy Daytee Maji Ishani Deb Source Type: research

Long non-coding RNA Gm11974 aggravates oxygen –glucose deprivation-induced injury via miR-122-5p/SEMA3A axis in ischaemic stroke
This study aimed to investigate the role and potential mechanism of lncRNA Gm11974 in ischaemic stroke. Mouse  neuroblastoma N2a cells were treated with oxygen–glucose deprivation (OGD). The levels of Gm11974, microRNA-122-5p (miR-122-5p) and semaphorin 3A (SEMA3A) were detected by quantitative real-time PCR (qRT-PCR) or western blot. Cell viability and apoptosis were determined by 3-(4,5-dimethyl-2-thia zolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, Caspase-3 Assay Kit and flow Cytometry. The levels of oxidative stress indicators were measured by using commercial kits. The relationship between miR-122-5p and ...
Source: Metabolic Brain Disease - August 2, 2021 Category: Neurology Source Type: research

Phenothiazines reduced autophagy in ischemic stroke through endoplasmic reticulum (ER) stress-associated PERK-eIF2 α pathway
CONCLUSION: The combined treatment of C + P plays a crucial role in stroke therapy by inhibiting ER stress-mediated autophagy, thereby leading to reduced apoptosis and increased neuroprotection. Our findings highlight the PERK-eIF2α pathway as a central mechanism through which C + P exerts its beneficial effects. The results from this study may pave the way for the development of more targeted and effective treatments for stroke patients.PMID:37673390 | DOI:10.1016/j.expneurol.2023.114524
Source: Experimental Neurology - September 6, 2023 Category: Neurology Authors: Shuyu Lv Xiaokun Geng Ho Jun Yun Yuchuan Ding Source Type: research

MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1
Monocyte locomotion inhibitory factor (MLIF) is a heat-stable pentapeptide from Entamoeba histolytica. Our previous study found that MLIF protects against ischemic stroke in rats and mice and exerts a neuroprotection effect in human neuroblastoma SH-SY5Y cells. Microglia/macrophage polarization has been proven to be vital in the pathology of ischemic stroke. Nevertheless, whether MLIF is able to modulate microglia/macrophage polarization remains unclear. We performed middle cerebral artery occlusion (MCAO) on C57BL/6J male mice and induced cultured BV2 microglia by oxygen-glucose deprivation (OGD), respectively. Immunfluor...
Source: Frontiers in Pharmacology - September 7, 2021 Category: Drugs & Pharmacology Source Type: research

Thiosulfate Mediates Cytoprotective Effects of Hydrogen Sulfide Against Neuronal Ischemia Stroke
Conclusions The protective effects of H2S are mediated by thiosulfate that is transported across cell membrane by NaS-2 and exerts antiapoptotic effects via persulfidation of caspase-3. Given the established safety track record, thiosulfate may be therapeutic against ischemic brain injury.
Source: JAHA:Journal of the American Heart Association - November 6, 2015 Category: Cardiology Authors: Marutani, E., Yamada, M., Ida, T., Tokuda, K., Ikeda, K., Kai, S., Shirozu, K., Hayashida, K., Kosugi, S., Hanaoka, K., Kaneki, M., Akaike, T., Ichinose, F. Tags: Stroke Source Type: research