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Condition: Ischemic Stroke

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Total 193 results found since Jan 2013.

Sirt1-Sirt3 axis regulates human blood-brain barrier permeability in response to ischemia
In this study, we investigated the role of Sirt1-Sirt3 axis in blood-brain barrier (BBB) permeability after ischemia in vitro. Human brain microvascular endothelial cells and astrocytes were co-cultured to model the BBB in vitro and oxygen and glucose deprivation (OGD) was performed to mimic ischemia. The results of transepithelial electrical resistance (TEER) showed that suppression of Sirt1 via siRNA or salermide significantly decreased BBB permeability, whereas Sirt3 knockdown increased BBB permeability. In addition, Sirt1 was shown to regulate Sirt3 expression after OGD through inhibiting the AMPK-PGC1 pathway. Applica...
Source: Redox Biology - September 29, 2017 Category: Biology Source Type: research

Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia
This study investigated the protective effects of N ′-(1-(2-((4-(4,4,5,5-tetramethyl-1,2,3-dioxoborolan-2-yl)benzyl)oxy)phenyl)ethylidene (BHAPI) on an in vitro ischemia model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. The results showed that BHAPI significantly increased cell viability and decreased lactate dehydrogen ase (LDH) release after OGD. BHAPI treatment also reduced apoptosis, as measured by flow cytometry, and suppressed caspase-3 activation. These protective effects were accompanied by preserved mitochondrial membrane potential (MMP), reduced mitochondrial swelling, promoted mito...
Source: Journal of Molecular Neuroscience - September 26, 2017 Category: Neuroscience Source Type: research

PTPN21 protects PC12 cell against oxygen-glucose deprivation by activating cdk5 through ERK1/2 signaling pathway.
In this study, we investigated the neuroprotective effects and potential mechanism of PTPN21 on oxygen glucose deprivation (OGD)-injured PC12 cells. The ischemic stroke model of PC12 cells was made by OGD for 2h, after transfection of the PTPN21 siRNA and pcDNA 3.1 PTPN21(+). Cell viability was tested using the MTT and CCK-8 assay. Apoptotic cells were estimated by Annexin V-FITC/PI staining and caspase-3 activity using the Caspase-3 Assay Kit; the PTPN21, cdk5, ERK1/2 and p-ERK1/2 levels were estimated by qRT-PCR and Western blot. We found that the PTPN21 markedly increased cell viability, inhibited apoptosis. We also fou...
Source: European Journal of Pharmacology - August 23, 2017 Category: Drugs & Pharmacology Authors: Cui N, Lu H, Li M, Yan Q Tags: Eur J Pharmacol Source Type: research

Long Noncoding RNA H19 Promotes Neuroinflammation in Ischemic Stroke by Driving Histone Deacetylase 1-Dependent M1 Microglial Polarization Basic Sciences
Conclusions—Our findings indicate that H19 promotes neuroinflammation by driving HDAC1-dependent M1 microglial polarization, suggesting a novel H19-based diagnosis and therapy for ischemic stroke.
Source: Stroke - July 24, 2017 Category: Neurology Authors: Jue Wang, Haiping Zhao, Zhibin Fan, Guangwen Li, Qingfeng Ma, Zhen Tao, Rongliang Wang, Juan Feng, Yumin Luo Tags: Animal Models of Human Disease, Cerebrovascular Disease/Stroke, Ischemic Stroke Original Contributions Source Type: research

Tumor necrosis factor receptor ‐associated factor 6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH using a Sprague–Dawley rat model of SAH induced in 0.3 mL non‐heparinized autologous arterial blood injected into the pre‐chiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 over‐expression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve...
Source: Journal of Neurochemistry - June 20, 2017 Category: Neuroscience Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research

Succinate-induced neuronal mitochondrial fission and hexokinase II malfunction in ischemic stroke: Therapeutical effects of kaempferol
This study indicates that succinate accumulation plays a pivotal role in I/R injury-induced neuronal mitochondrial dysfunction, and suggests that modulation of Drp1 phosphorylation might be potential therapeutic strategy to protect neuron mitochondrial integrity and treat ischemic stroke.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - June 19, 2017 Category: Molecular Biology Source Type: research

Prdx6 Upregulation by Curcumin Attenuates Ischemic Oxidative Damage via SP1 in Rats after Stroke.
CONCLUSIONS: Prdx6 upregulation by Cur treatment attenuates ischemic oxidative damage through SP1 induction in rats after stroke. This represents a novel mechanism of Cur-induced neuroprotection against cerebral ischemia. PMID: 28596967 [PubMed - in process]
Source: Biomed Res - June 10, 2017 Category: Research Authors: Jia G, Tan B, Ma J, Zhang L, Jin X, Li C Tags: Biomed Res Int Source Type: research

TRAF6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH by using a Sprague–Dawley rat model of SAH induced in 0.3 ml non‐heparinized autologous arterial blood injected into the prechiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 overexpression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve EBI ...
Source: Journal of Neurochemistry - May 24, 2017 Category: Neurology Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research

Neuroprotective Effects of Sulfiredoxin-1 During Cerebral Ischemia/Reperfusion Oxidative Stress Injury in Rats.
Abstract As an endogenous antioxidant protein, Sulfiredoxin1 (Srxn1) can prevent cell oxidative stress damage. However, its role in cerebral ischemia/reperfusion (I/R) injury and the underlying signaling mechanisms remain largely unknown. Here, we explored effects of Srxn1 knockdown on oxidative stress using in vitro and in vivo I/R models and investigated related neuroprotective mechanisms. For in vitro studies, primary cortical neuronal cultures were transfected with an interfering lentivirus targeting Srxn1. Oxygen-glucose deprivation (OGD) was conducted after Srxn1 knockdown. MTS and lactate dehydrogenase assa...
Source: Brain Research Bulletin - May 24, 2017 Category: Neurology Authors: Wu J, Chen Y, Yu S, Li L, Zhao X, Li Q, Zhao J, Zhao Y Tags: Brain Res Bull Source Type: research

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD+/Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats Basic Sciences
Conclusions—HBO induced activation of ATP/nicotinamide adenine dinucleotide/silent mating type information regulation 2 homolog 1 pathway and protected blood–brain barrier in hyperglycemic middle cerebral artery occlusion rats. HBO might be promising approach for treatment of acute ischemic stroke patients, especially patients with diabetes mellitus or treated with r-tPA (recombinant tissue-type plasminogen activator).
Source: Stroke - May 22, 2017 Category: Neurology Authors: Qin Hu, Anatol Manaenko, Hetao Bian, Zongduo Guo, Jun-Long Huang, Zhen-Ni Guo, Peng Yang, Jiping Tang, John H. Zhang Tags: Animal Models of Human Disease, Basic Science Research, Ischemia, Neuroprotectants Original Contributions Source Type: research

The 15-LO-1/15-HETE system promotes angiogenesis by upregulating VEGF in ischemic brains.
DISCUSSION: The results indicate that the 15-LO-1/15-HETE system promotes angiogenesis in ischemic brains by upregulation of VEGF, representing a potential target for improving neurobehavioral recovery after cerebral ischemic stroke. PMID: 28460604 [PubMed - as supplied by publisher]
Source: Neurological Research - May 5, 2017 Category: Neurology Tags: Neurol Res Source Type: research

TDAG8 activation attenuates cerebral ischaemia-reperfusion injury via Akt signalling in rats.
CONCLUSIONS: TDAG8 plays an important neuroprotective role through inhibition of neuronal apoptosis and alleviation of neurological deficits by activating the Akt signalling pathway in rats. PMID: 28365474 [PubMed - as supplied by publisher]
Source: Experimental Neurology - March 29, 2017 Category: Neurology Authors: Ma XD, Hang LH, Shao DH, Shu WW, Hu XL, Luo H Tags: Exp Neurol Source Type: research

TGF- β1/Smad3 Signaling Pathway Suppresses Cell Apoptosis in Cerebral Ischemic Stroke Rats.
CONCLUSIONS The TGF-β1/Smad3 signaling pathway was up-regulated once cerebral ischemic stroke was simulated. TGF-β1 may activate the expression of Bcl-2 via Smad3 to suppress the apoptosis of neurons. PMID: 28110342 [PubMed - in process]
Source: Medical Science Monitor - January 25, 2017 Category: Research Tags: Med Sci Monit Source Type: research

Cystatin C Is a Crucial Endogenous Protective Determinant Against Stroke Basic Sciences
Conclusions—CysC is a crucial determinant contributing to endogenous neuroprotection. It is also a novel candidate for stroke treatment through maintaining lysosomal membrane integrity.
Source: Stroke - January 22, 2017 Category: Neurology Authors: Zongping Fang, Jiao Deng, Zhixin Wu, Beibei Dong, Shiquan Wang, Xiaodan Chen, Huang Nie, Hailong Dong, Lize Xiong Tags: Ischemic Stroke, Neuroprotectants Original Contributions Source Type: research

Influence of miR-155 on Cell Apoptosis in Rats with Ischemic Stroke: Role of the Ras Homolog Enriched in Brain (Rheb)/mTOR Pathway.
CONCLUSIONS Inhibition of miR-155 may play protective roles in ischemic stroke by phosphorylating S6K through the Rheb/mTOR pathway. PMID: 28025572 [PubMed - in process]
Source: Medical Science Monitor - December 28, 2016 Category: Research Tags: Med Sci Monit Source Type: research