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Condition: Stroke

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Total 302 results found since Jan 2013.

Hes1 Knockdown Exacerbates Ischemic Stroke Following tMCAO by Increasing ER Stress-Dependent Apoptosis via the PERK/eIF2 α/ATF4/CHOP Signaling Pathway
In this study, using a mouse model of ischemic strokevia transient middle cerebral artery occlusion (tMCAO), we found that Hes1 was induced following brain injury, and that siRNA-mediated knockdown of Hes1 increased the cerebral infarction and worsened the neurological outcome, suggesting that Hes1 knockdown exacerbates ischemic stroke. In addition, mechanistically, Hes1 knockdown promoted apoptosis and activated the PERK/eIF2 α/ATF4/CHOP signaling pathway after tMCAO. These results suggest that Hes1 knockdown promotes ER stress-induced apoptosis. Furthermore, inhibition of PERK with the specific inhibitor GSK2606414 mark...
Source: Neuroscience Bulletin - January 23, 2020 Category: Neuroscience Source Type: research

ACOX3 Dysfunction as a Potential Cause of Recurrent Spontaneous Vasospasm of Internal Carotid Artery
AbstractRecurrent spontaneous vasospasm of the extracranial internal carotid artery (RSV-eICA) is a rarely recognized cause of ischemic stroke in young adults. However, its pathophysiology remains largely unknown. Through whole-exome sequencing of the ACOX3 gene of two dizygotic Korean twin brothers affected by RSV-eICA, we identified two compound heterozygous missense variants c.235  T >  G (p.F79 V) and c.665G >  A (p.G222E). In silico analysis indicated that both variants were classified as pathogenic. In vitro ACOX3 enzyme assay indicated practically no enzyme activity in both F79 V and G222E mutants. ...
Source: Translational Stroke Research - January 22, 2020 Category: Neurology Source Type: research

MALAT1 affects hypoxia-induced vascular endothelial cell injury and autophagy by regulating miR-19b-3p/HIF-1 α axis.
MALAT1 affects hypoxia-induced vascular endothelial cell injury and autophagy by regulating miR-19b-3p/HIF-1α axis. Mol Cell Biochem. 2020 Jan 13;: Authors: Liu H, Shi C, Deng Y Abstract Cardiovascular disease has become the leading cause of death in the world. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in cardiovascular disease, such as stroke. However, the role of MALAT1 in hypoxia (HYP)-induced vascular endothelial cells (VECs) remains unclear. In the present study, HYP-treated human umbilical vein endothelial cells (HUVECs) were utilized to simulate HY...
Source: Molecular and Cellular Biochemistry - January 12, 2020 Category: Biochemistry Authors: Liu H, Shi C, Deng Y Tags: Mol Cell Biochem Source Type: research

Recombinant OX40 attenuates neuronal apoptosis through OX40-OX40L/PI3K/AKT signaling pathway following subarachnoid hemorrhage in rats.
Abstract Subarachnoid hemorrhage (SAH) is the most devastating form of stroke. Reducing neuronal apoptosis is an important countermeasure against early brain injury (EBI) after SAH. Recent evidence indicates that OX40-OX40L coupling is critical for cell survival and proliferation. Current study was performed to detect the role of recombinant OX40 (ReOX40) against neuronal apoptosis after SAH. The endovascular perforation model of SAH was performed on Sprague-Dawley (SD) rats. ReOX40 was injected intracerebroventricularly (i.c.v) 1 h after SAH induction and the following methods were employed: neurological functi...
Source: Experimental Neurology - January 9, 2020 Category: Neurology Authors: Wu LY, Enkhjargal B, Xie ZY, Travis ZD, Sun CM, Zhou KR, Zhang TY, Zhu QQ, Hang CH, Zhang JH Tags: Exp Neurol Source Type: research

Inhibition of TRIM8 restrains ischaemia-reperfusion-mediated cerebral injury by regulation of NF- κB activation associated inflammation and apoptosis.
Inhibition of TRIM8 restrains ischaemia-reperfusion-mediated cerebral injury by regulation of NF-κB activation associated inflammation and apoptosis. Exp Cell Res. 2020 Jan 06;:111818 Authors: Bai X, Zhang YL, Liu LN Abstract Stroke is a leading global cause of mortality and disability. However, the pathogenesis that contributes to stroke has not been fully understood. The tripartite motif (TRIM)-containing proteins usually exhibit essential regulatory roles during various biological processes. TRIM8 is a RING domain-containing E3 ubiquitin ligase, playing crucial roles in regulating inflammation and...
Source: Experimental Cell Research - January 5, 2020 Category: Cytology Authors: Bai X, Zhang YL, Liu LN Tags: Exp Cell Res Source Type: research

Intranasal wnt-3a alleviates neuronal apoptosis in early brain injury post subarachnoid hemorrhage via the regulation of wnt target PPAN mediated by the moonlighting role of aldolase C
Publication date: Available online 31 December 2019Source: Neurochemistry InternationalAuthor(s): Wu Ruan, Junwen Hu, Hang Zhou, Yin Li, Chaoran Xu, Yujie Luo, Ting Chen, Bangliang Xu, Feng Yan, Gao ChenAbstractNeuronal apoptosis is one of the main pathophysiological events in the early brain injury (EBI) post subarachnoid hemorrhage (SAH). Wnt-3a, one of the endogenous wnt ligands crucial in neurogenesis, has been proven to be efficacious in neuroprotection in traumatic brain injury and ischemic stroke. The glycolytic enzyme aldolase C and ribosome biogenesis protein PPAN were revealed to be linked to wnt signaling pathwa...
Source: Neurochemistry International - January 1, 2020 Category: Neuroscience Source Type: research

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.
Abstract Allopurinol (ALP) attenuates oxidative stress and diabetic cardiomyopathy (DCM), but the mechanism is unclear. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) following the disassociation with its repressor Keap1 under oxidative stress can maintain inner redox homeostasis and attenuate DCM with concomitant attenuation of autophagy. We postulated that ALP treatment may activate Nrf2 to mitigate autophagy over-activation and consequently attenuate DCM. Streptozotocin-induced type 1 diabetic rats were untreated or treated with ALP (100 mg/kg/d) for 4 weeks and terminated after heart functi...
Source: J Cell Mol Med - December 18, 2019 Category: Molecular Biology Authors: Luo J, Yan D, Li S, Liu S, Zeng F, Cheung CW, Liu H, Irwin MG, Huang H, Xia Z Tags: J Cell Mol Med Source Type: research

Silencing of TXNIP Alleviated Oxidative Stress Injury by Regulating MAPK-Nrf2 Axis in Ischemic Stroke.
This study aimed to investigate the underlying molecular mechanism and propose the potential therapeutic strategy for ischemic stroke. Bioinformatics analysis based on a public microarray profile (GSE 61616) of ischemic stroke rats was performed as a pilot research. Oxidative stress was enriched as a significantly gene ontology item, and thioredoxin-interacting protein (TXNIP) and MAPK signaling were identified as the hub gene and pathway, respectively. The experiments in middle cerebral artery occlusion rats demonstrated that ischemia induced the activation of oxidative stress. The expressions of TXNIP, p-p38, p-JNK, p-ER...
Source: Neurochemical Research - December 18, 2019 Category: Neuroscience Authors: Tian Y, Su Y, Ye Q, Chen L, Yuan F, Wang Z Tags: Neurochem Res Source Type: research

Pseudoginsenoside-F11 Accelerates Microglial Phagocytosis of Myelin Debris and Attenuates Cerebral Ischemic Injury Through Complement Receptor 3
Publication date: Available online 29 November 2019Source: NeuroscienceAuthor(s): Yinglu Liu, Chunfu Wu, Zongjuan Hou, Xiaoxiao Fu, Linlin Yuan, Shibo Sun, Haotian Zhang, Depeng Yang, Xuechun Yao, Jingyu YangAbstractAfter ischemic stroke, the degenerated myelin caused by ischemic injury cannot be rapidly cleared away by microglia and interferes with the recovery process. Complement receptor 3 (CR3, CD11b/CD18), belonging to β2 integrin family primarily expressed in phagocytes, is involved in the microglial phagocytosis of myelin debris. We previously found that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, exer...
Source: Neuroscience - November 30, 2019 Category: Neuroscience Source Type: research

Delivery of High Mobility Group Box-1 siRNA Using Brain-Targeting Exosomes for Ischemic Stroke Therapy
Source: Journal of Biomedical Nanotechnology - November 22, 2019 Category: Nanotechnology Authors: Kim, Minkyung Kim, Gyeungyun Hwang, Do Won Lee, Minhyung Tags: Articles Source Type: research

Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Ppar γ), and elastin-binding protein (EBP).
Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Pparγ), and elastin-binding protein (EBP). Cytokine. 2019 Nov 21;126:154930 Authors: Szychowski KA, Gmiński J Abstract During aging and ischemic and hemorrhagic stroke, elastin molecules are degraded and elastin-derived peptides are released into the brain microenvironment. Val-Gly-Val-Ala-Pro-Gly (VGVAPG) is a repeating hexapeptide in the elastin molecule. It is well documented that the peptide sequence binds...
Source: Cytokine - November 20, 2019 Category: Molecular Biology Authors: Szychowski KA, Gmiński J Tags: Cytokine Source Type: research

GAS5 knockdown ameliorates apoptosis and inflammatory response by modulating miR-26b-5p/Smad1 axis in cerebral ischaemia/reperfusion injury.
This study established a CI / R injury model in vivo and in vitro. The results showed that the expression of GAS5 was increased in CI / R rats, while miR-26b-5p expression was decreased. Besides, knockdown of GAS5 by siRNA (si-GAS5) reversed CI / R-induced apoptosis and inflammatory responses. Notably, bioinformatics analysis indicated that GAS5 competitively adsorbed miR-26b-5p, and the relationship was further confirmed by pull-down assay. In addition, miR-26b-5p overexpression reversed CI / R-induced apoptosis and inflammatory responses, whereas low expression of miR-26b-5p had the opposite effect. Moreover, TargetScan ...
Source: Behavioural Brain Research - November 17, 2019 Category: Neurology Authors: Shangguan Y, Han J, Su H Tags: Behav Brain Res Source Type: research

Deletion of Chitinase-3-like 1 accelerates stroke development through enhancement of Neuroinflammation by STAT6-dependent M2 microglial inactivation in Chitinase-3-like 1 knockout mice.
Abstract Chitinase 3-like 1 (Chi3L1) plays a major role in the pathogenesis of inflammatory diseases. We investigated the effect of Chi3L1 knockout on stroke development. Ischemia/reperfusion was induced by middle cerebral artery occlusion (MCAO) in Chi3L1 knockout and wildtype mice. Significantly increased infarct volume and decreased neurological deficit scores at 24 h after ischemia/reperfusion were found in Chi3L1 knockout mice compared to wildtype mice. Moreover, ischemic neuronal cell death was increased in Chi3L1 knockout mice through increased oxidative stress and release of IL-6 and IL-1β but IL-10 and...
Source: Experimental Neurology - October 23, 2019 Category: Neurology Authors: Im JH, Yeo IJ, Park PH, Choi DY, Han SB, Yun J, Hong JT Tags: Exp Neurol Source Type: research

Cystatin C Improves Blood ‐Brain Barrier Integrity After Ischemic Brain Injury in Mice
AbstractCystatin C, a well ‐established biomarker of renal function, has been associated with a protective effect against stroke. However, the potential neuroprotective mechanism of cystatin C in ischemic brain injury remains unclear. Our study hypothesized that cystatin C can ameliorate blood‐brain barrier (BBB) disrupti on by upregulating caveolin‐1 expression, thereby improving neurological outcomes in cerebral ischemic injury. Western blotting, immunohistochemistry, immunofluorescence staining, and immunoprecipitation were performed to investigate target proteins. Evans Blue and gelatin zymography were used to ex...
Source: Journal of Neurochemistry - October 10, 2019 Category: Neuroscience Authors: Bo Yang, Junjie Xu, Liuhui Chang, Zhigang Miao, Dara Heang, Yuwei Pu, Xun Zhou, Lingwei Zhang, Hong Xie Tags: ORIGINAL ARTICLE Source Type: research

Aggravation of Cerebral Ischemia/Reperfusion Injury by Peroxisome Proliferator-Activated Receptor-Gamma Deficiency via Endoplasmic Reticulum Stress.
CONCLUSIONS This research proved that PPAR-γ protected the brain from cerebral I/R injury by repressing ER stress and indicated that PPAR-γ is a potential target in the treatment of ischemia. PMID: 31588926 [PubMed - in process]
Source: Medical Science Monitor - October 9, 2019 Category: Research Tags: Med Sci Monit Source Type: research