5,536 results match your criteria Reperfusion Injury in Stroke


tiRNAs as a Novel Biomarker for Cell Damage Assessment in In Vitro Ischemia-Reperfusion Model in Rat Neuronal PC12 Cells.

Brain Res 2019 Feb 16. Epub 2019 Feb 16.

Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan.

The disruption of appropriate cellular stress responses is implicated in the pathogenesis of different neurological disorders including ischemic injury. Early diagnosis and treatment are often associated with better prognosis in ischemic stroke patients. Thus, there is an urgent need to improve the speed and accuracy of stroke diagnosis by developing highly sensitive stroke biomarkers. Read More

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http://dx.doi.org/10.1016/j.brainres.2019.02.019DOI Listing
February 2019

miR-1247-3p mediates apoptosis of cerebral neurons by targeting caspase-2 in stroke.

Brain Res 2019 Feb 16. Epub 2019 Feb 16.

New Drug Innovation and Development Institute, Department of Pharmacy, College of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei Province, China; Department of Biomedical Engineering, School of Medicine and School of Engineering, The University of Alabama at Birmingham, USA; Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, Hubei Province, China. Electronic address:

Brain stroke is one of the leading causes of death worldwide. We explored a potential stroke-related role for a newly found microRNA, miR-1247-3p, and one of its target genes, caspase-2, predicted by TargetScanVert. In the present study, we found that miR-1247-3p was downregulated during ischemia/reperfusion (I/R) and that LV-miR-1247-3p overexpression attenuated brain impairment induced by I/R. Read More

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http://dx.doi.org/10.1016/j.brainres.2019.02.020DOI Listing
February 2019

Tumour Necrosis Factor-α Inhibition Improves Stroke Outcome in a Mouse Model of Rheumatoid Arthritis.

Sci Rep 2019 Feb 18;9(1):2173. Epub 2019 Feb 18.

Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland.

Rheumatoid Arthritis (RA) is a chronic inflammatory disorder where incidence and severity of myocardial infarction are increased. Data on the incidence and outcome of stroke are conflicting. Thus, we investigated outcome after Ischemia/Reperfusion (I/R) brain injury in a mouse model of RA and assessed for the role of the tumour necrosis factor-α (TNF-α) inhibitor Infliximab herein. Read More

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http://dx.doi.org/10.1038/s41598-019-38670-zDOI Listing
February 2019

Mural cell-derived laminin-α5 plays a detrimental role in ischemic stroke.

Acta Neuropathol Commun 2019 Feb 18;7(1):23. Epub 2019 Feb 18.

Department of Pharmaceutical and Biomedical Sciences, University of Georgia, 240 W Green Street, Athens, GA, 30602, USA.

At the blood-brain barrier (BBB), laminin-α5 is predominantly synthesized by endothelial cells and mural cells. Endothelial laminin-α5 is dispensable for BBB maintenance under homeostatic conditions but inhibits inflammatory cell extravasation in pathological conditions. Whether mural cell-derived laminin-α5 is involved in vascular integrity regulation, however, remains unknown. Read More

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http://dx.doi.org/10.1186/s40478-019-0676-8DOI Listing
February 2019

Expression and regulation of miR-449a and AREG in cerebral ischemic injury.

Metab Brain Dis 2019 Feb 18. Epub 2019 Feb 18.

Department of Ophthalmology, Affiliated Hospital of ChiFeng University, ChiFeng, 024000, China.

Rodent focal ischemia models are widely used to mimic and examine human strokes. To the best of our knowledge, no investigation has systematically examined the expression changes of microRNA (miR)-449a and Amphiregulin (AREG) as well as their biological relationship during middle cerebral artery occlusion (MCAO) and oxygen and glucose deprivation/reperfusion (OGD/R). The present study examined the histological and behavioral outcomes of MCAO and the function of miR-449a and AREG in cerebral ischemic injury. Read More

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http://dx.doi.org/10.1007/s11011-019-0393-9DOI Listing
February 2019

Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke.

Neural Regen Res 2019 Jun;14(6):948-953

Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.

Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however, excess reactive oxygen species generated by NOX promotes apoptotic cell death. Read More

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http://dx.doi.org/10.4103/1673-5374.250568DOI Listing

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro.

Neurochem Res 2019 Feb 13. Epub 2019 Feb 13.

Department of Clinical Biochemistry and Laboratory Diagnostics, Institute of Medicine, University of Opole, Oleska 48, 45-052, Opole, Poland.

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) and neuronal nitric oxide synthase (nNos) in mouse cortical astrocytes in vitro. Read More

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http://dx.doi.org/10.1007/s11064-019-02746-zDOI Listing
February 2019

Neuroprotective Effect of Swertiamain on Cerebral Ischemia/Reperfusion Injury by Inducing the Nrf2 Protective Pathway.

ACS Chem Neurosci 2019 Feb 19. Epub 2019 Feb 19.

Department of Pharmacology, College of Pharmacy , Ningxia Medical University , Yinchuan , Ningxia Hui Autonomous Region 750004 , P.R. China.

Oxidative stress plays a vital role in the development of cerebral ischemic/reperfusion (I/R). Targeting oxidative stress is proposed to be an effective strategy to treat cerebral I/R injury. Gentiana macrophylla Pall is reported to have a potential protective effect against stroke. Read More

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http://pubs.acs.org/doi/10.1021/acschemneuro.8b00605
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http://dx.doi.org/10.1021/acschemneuro.8b00605DOI Listing
February 2019
2 Reads

Ischemia-induced ACSL4 activation contributes to ferroptosis-mediated tissue injury in intestinal ischemia/reperfusion.

Cell Death Differ 2019 Feb 8. Epub 2019 Feb 8.

Department of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.

Ferroptosis is a recently identified form of regulated cell death defined by the iron-dependent accumulation of lipid reactive oxygen species. Ferroptosis has been studied in various diseases such as cancer, Parkinson's disease, and stroke. However, the exact function and mechanism of ferroptosis in ischemia/reperfusion (I/R) injury, especially in the intestine, remains unknown. Read More

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http://dx.doi.org/10.1038/s41418-019-0299-4DOI Listing
February 2019
2 Reads

Response by Gauberti et al to Letter Regarding Article, "Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke".

Stroke 2019 Feb 7:STROKEAHA118024503. Epub 2019 Feb 7.

Normandie University, UNICAEN, INSERM, INSERM UMR-S U1237, Physiopathology and Imaging of Neurological Disorders, Caen, France.

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http://dx.doi.org/10.1161/STROKEAHA.118.024503DOI Listing
February 2019

Letter by Desilles et al Regarding Article, "Ischemia-Reperfusion Injury After Endovascular Thrombectomy for Ischemic Stroke".

Stroke 2019 Feb 7:STROKEAHA118024391. Epub 2019 Feb 7.

Laboratory of Vascular Translational Science, Université Paris Diderot, Sorbonne Paris Cite, U1148 Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.

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http://dx.doi.org/10.1161/STROKEAHA.118.024391DOI Listing
February 2019

Alpha-1 Antitrypsin Substitution for Extrapulmonary Conditions in Alpha-1 Antitrypsin Deficient Patients.

Chronic Obstr Pulm Dis 2018 Sep 19;5(4):267-276. Epub 2018 Sep 19.

Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder which most commonly manifests as pulmonary emphysema. Accordingly, alpha-1 antitrypsin (AAT) augmentation therapy aims to reduce the progression of emphysema, as achieved by life-long weekly slow-drip infusions of plasma-derived affinity-purified human AAT. However, not all AATD patients will receive this therapy, due to either lack of medical coverage or low patient compliance. Read More

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http://dx.doi.org/10.15326/jcopdf.5.4.2017.0161DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6361480PMC
September 2018
2 Reads

Intraoperative Hemodynamic Parameters and Acute Kidney Injury After Living Donor Liver Transplantation.

Transplantation 2019 Jan 30. Epub 2019 Jan 30.

Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul, Republic of Korea.

Background: Acute kidney injury (AKI) after living donor liver transplantation (LDLT) is associated with increased mortality. We sought to identify associations between intraoperative hemodynamic variables and postoperative AKI.

Methods: We retrospectively reviewed 734 cases of LDLT. Read More

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http://dx.doi.org/10.1097/TP.0000000000002584DOI Listing
January 2019
1 Read

Erythropoietin Pretreatment Effect on Blood Glucose and Its Relationship With Inflammatory Factors After Brain Ischemic-Reperfusion Injury in Rats.

Basic Clin Neurosci 2018 Sep-Oct;9(5):347-356. Epub 2018 Sep 1.

Department of Physiology and Pharmacology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

Introduction: Brain Ichemic-Reperfusion Injury (IRI) activates different pathophysiological processes. It also changes physiological parameters such as Blood Glucose (BG) level. An increase in BG after stroke is associated with poor clinical outcomes. Read More

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http://dx.doi.org/10.32598/bcn.9.5.347DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6360489PMC
September 2018
1 Read

MEPO promotes neurogenesis and angiogenesis but suppresses gliogenesis in mice with acute ischemic stroke.

Eur J Pharmacol 2019 Feb 2;849:1-10. Epub 2019 Feb 2.

Institute of Cerebrovascular Disease Research and Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China; Beijing Geriatric Medical Research Center and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China; Beijing Institute for Brain Disorders, Beijing, China. Electronic address:

Previously study has proved the non-erythropoietic mutant erythropoietin (MEPO) exerted neuroprotective effects against ischemic cerebral injury, with an efficacy similar to that of wild-type EPO. This study investigates its effects on neurogenesis, angiogenesis, and gliogenesis in cerebral ischemic mice. Male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO) and reperfusion. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00142999193003
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http://dx.doi.org/10.1016/j.ejphar.2019.01.066DOI Listing
February 2019
3 Reads

Causes and consequences of microRNA dysregulation following cerebral ischemia-reperfusion injury.

CNS Neurol Disord Drug Targets 2019 Feb 3. Epub 2019 Feb 3.

UKM Medical Centre (HUKM), Department of Medicine, Faculty of Medicine. Malaysia.

Stroke continues to be a major cause of death and disability worldwide. In this respect, the most important mechanisms underlying stroke pathophysiology are inflammatory pathways, oxidative stress, as well as apoptosis. Accordingly, miRNAs are considered as non-coding endogenous RNA molecules interacting with their target mRNAs to inhibit mRNA translation or reduce its transcription. Read More

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http://www.eurekaselect.com/169590/article
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http://dx.doi.org/10.2174/1871527318666190204104629DOI Listing
February 2019
7 Reads

Proteomic Analysis of Hydroxysafflor Yellow A against Cerebral Ischemia-Reperfusion Injury in Rats.

Rejuvenation Res 2019 Feb 2. Epub 2019 Feb 2.

Xijing Hospital, Fourth Military Medical University, Department of pharmacy , Changle West Street 15, Xi'an, Shaanxi 710032, China , Xian, China , 710032 ;

Ischemic stroke is a common cerebrovascular disease with high morbidity and mortality worldwide. However, treatment options for reducing cerebral ischemia-reperfusion injury (CIRI) are limited. Gallic acid (GA) as a plant polyphenol has been used to fight against CIRI. Read More

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http://dx.doi.org/10.1089/rej.2018.2145DOI Listing
February 2019
2 Reads

Glycine Exhibits Neuroprotective Effects in Ischemic Stroke in Rats through the Inhibition of M1 Microglial Polarization via the NF-κB p65/Hif-1α Signaling Pathway.

J Immunol 2019 Feb 1. Epub 2019 Feb 1.

Institute of Neuroregeneration and Neurorehabilitation, Department of Neurosurgery of the Affiliated Hospital, Qingdao University, Qingdao 266071, China

Glycine is a simple nonessential amino acid known to have neuroprotective properties. Treatment with glycine results in reduced infarct volume of the brain, neurologic function scores, and neuronal and microglial death in ischemic stroke injury. Neuroinflammation has been considered a major contributor to cerebral ischemia-induced brain damage. Read More

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http://dx.doi.org/10.4049/jimmunol.1801166DOI Listing
February 2019
4.922 Impact Factor

Neuroprotective effect of Apelin 13 on ischemic stroke by activating AMPK/GSK-3β/Nrf2 signaling.

J Neuroinflammation 2019 Feb 1;16(1):24. Epub 2019 Feb 1.

Department of Pharmacy, Xijing Hospital, Air Force Medical University, No. 127, Changle West Road, Xi'an, 710032, Shaanxi, China.

Background: Previous studies had showed that Apelin 13 could protect against apoptosis induced by ischemic/reperfusion (I/R). However, the mechanisms whereby Apelin 13 protected brain I/R remained to be elucidated. The present study was designed to determine whether Apelin 13 provided protection through AMPK/GSK-3β/Nrf2 pathway. Read More

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http://dx.doi.org/10.1186/s12974-019-1406-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357442PMC
February 2019
1 Read

Local and systemic metabolic alterations in brain, plasma, and liver of rats in response to aging and ischemic stroke, as detected by nuclear magnetic resonance (NMR) spectroscopy.

Neurochem Int 2019 Jan 30. Epub 2019 Jan 30.

Department of Neurological Surgery, University of Wisconsin, Madison, WI, 53792, USA.

Metabolic dysfunction impacts stroke incidence and outcome. However, the intricate association between altered metabolic program due to aging, and focal ischemia in brain, circulation, and peripheral organs is not completely elucidated. Here we identified locally and systemically altered metabolites in brain, liver, and plasma as a result of normal aging, ischemic-stroke, and extended time of reperfusion injury. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.01.025DOI Listing
January 2019

Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1.

Exp Neurol 2019 Apr 29;314:100-110. Epub 2019 Jan 29.

Department of Emergency Medicine, The First Affiliated Hospital of Kunming Medical University, No. 295 Xichang Road, Wu Hua District, Kunming 650032, Yunnan Province, China. Electronic address:

Emerging evidence has suggested a significant role of long non-coding RNAs (lncRNAs) in ischemic stroke by acting as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs) to regulate certain RNA transcripts. AK038897 is an lncRNA that was reported to be upregulated in rat brains in response to transient focal ischemia. We aimed to investigate the possible regulatory role of AK038897 in ischemic stroke. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00144886183039
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http://dx.doi.org/10.1016/j.expneurol.2019.01.009DOI Listing
April 2019
3 Reads
4.696 Impact Factor

White Matter Integrity and Early Outcomes After Acute Ischemic Stroke.

Transl Stroke Res 2019 Jan 28. Epub 2019 Jan 28.

J. Philip Kistler Stroke Research Center, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, 175 Cambridge Street, Suite 300, Boston, MA, 02114, USA.

Chronic white matter structural injury is a risk factor for poor long-term outcomes after acute ischemic stroke (AIS). However, it is unclear how white matter structural injury predisposes to poor outcomes after AIS. To explore this question, in 42 AIS patients with moderate to severe white matter hyperintensity (WMH) burden, we characterized WMH and normal-appearing white matter (NAWM) diffusivity anisotropy metrics in the hemisphere contralateral to acute ischemia in relation to ischemic tissue and early functional outcomes. Read More

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http://dx.doi.org/10.1007/s12975-019-0689-4DOI Listing
January 2019
1 Read

A Linear Fragment of Unacylated Ghrelin (UAG) Protects Against Myocardial Ischemia/Reperfusion Injury in Mice in a Growth Hormone Secretagogue Receptor-Independent Manner.

Front Endocrinol (Lausanne) 2018 11;9:798. Epub 2019 Jan 11.

Faculté de pharmacie, Université de Montréal, Montréal, QC, Canada.

Unacylated ghrelin (UAG), the most abundant form of ghrelin in circulation, has been shown to exert cardioprotective effect in experimental cardiopathies. The present study aimed to investigate the cardioprotective effect of a linear bioactive fragment of UAG against myocardial ischemia-induced injury and dysfunction in C57BL/6 wild type mice and the mechanisms involved. Treatments were administered at doses of 100 (UAG), 1,000 and 3,000 (UAG) nmol/kg at 12 h interval during 14 days prior to 30 min left coronary artery ligation and reperfusion for a period of 6 or 48 h. Read More

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https://www.frontiersin.org/article/10.3389/fendo.2018.00798
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http://dx.doi.org/10.3389/fendo.2018.00798DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6340090PMC
January 2019
4 Reads

ESE1 expression correlates with neuronal apoptosis in the hippocampus after cerebral ischemia/reperfusion injury.

Neural Regen Res 2019 May;14(5):841-849

Clinical Medical College of Yangzhou University; Department of Neurology, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu Province, China.

Epithelial-specific ETS-1 (ESE1), a member of the ETS transcription factor family, is widely expressed in multiple tissues and performs various functions in inflammation. During neuroinflammation, ESE1 promotes neuronal apoptosis; however, the expression and biological functions of ESE1 remain unclear after cerebral ischemia/reperfusion. We performed in vivo and in vitro experiments to explore the role of ESE1 in cerebral ischemic injury. Read More

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http://dx.doi.org/10.4103/1673-5374.249232DOI Listing

Storax Protected Oxygen-Glucose Deprivation/Reoxygenation Induced Primary Astrocyte Injury by Inhibiting NF-κB Activation .

Front Pharmacol 2018 11;9:1527. Epub 2019 Jan 11.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Stroke is the second leading cause of death and the leading cause of long-term disability in the world. There is an urgent unmet need to develop a range of neuroprotective strategies to restrain the damage that occurs in the hours and days following a stroke. Storax, a natural resin extracted from injuring Mill, has been used to treat acute stroke in traditional Chinese medicine for many centuries. Read More

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http://dx.doi.org/10.3389/fphar.2018.01527DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337066PMC
January 2019

Neutrophil Membrane-Derived Nanovesicles Alleviate Inflammation To Protect Mouse Brain Injury from Ischemic Stroke.

ACS Nano 2019 Jan 28. Epub 2019 Jan 28.

Ischemic stroke is an acute and severe neurological disease, resulting in disability and death. Reperfusion to an ischemic brain is a means to reverse brain damage after stroke; however, this causes secondary tissue damage induced by inflammation responses, called ischemia/reperfusion (I/R) injury. Adhesion of neutrophils to endothelial cells underlies the initiation of inflammation in I/R. Read More

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http://dx.doi.org/10.1021/acsnano.8b06572DOI Listing
January 2019

Upregulation of miR-335 ameliorates myocardial ischemia reperfusion injury via targeting hypoxia inducible factor 1-alpha subunit inhibitor.

Am J Transl Res 2018 15;10(12):4082-4094. Epub 2018 Dec 15.

The Central Laboratory of The First Affiliated Hospital of China Medical University Shenyang, China.

MicroRNA-335 (miR-335) is implicated in several pathophysiological processes, including tumorigenesis, lipid metabolism and ischemic stroke; however, whether miR-335 plays a role in modulating myocardial ischemia reperfusion injury (MIRI) is still unknown. This study is aimed to explore the role and mechanism of miR-335 in the pathophysiological process of MIRI. Specifically, miR-335 mimics or a chemically modified agomiR-335 were transfected or injected into H9c2 cells and Wistar rats to upregulate miR-335 expression and , respectively. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325516PMC
December 2018
1 Read

Does the Apparent Diffusion Coefficient Value Predict Permanent Cerebral Ischemia/Reperfusion Injury in Rats?

Acad Radiol 2019 Jan 17. Epub 2019 Jan 17.

Asan Institute for Life Sciences, Asan Medical Center, Songpa-gu, Seoul, Republic of Korea. Electronic address:

Rationale And Objectives: Variation in tissue damage after cerebral ischemia/reperfusion (I/R) can cause uncertainty in stroke-related studies, which can be reduced if the damage can be predicted early after ischemia by measuring the apparent diffusion coefficient (ADC). We investigated whether ADC measurement in the acute phase can predict permanent cerebral I/R injury.

Materials And Methods: The middle cerebral artery occlusion model was established using the intraluminal suture method to induce 60 minutes of ischemia followed by reperfusion in rats. Read More

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http://dx.doi.org/10.1016/j.acra.2018.12.022DOI Listing
January 2019
2 Reads

Takotsubo cardiomyopathy and neurogenic pulmonary edema after carotid endarterectomy.

World Neurosurg 2019 Jan 17. Epub 2019 Jan 17.

Department of Neurosurgery, Brain Attack Center, Ota Memorial Hospital, Fukuyama, Hiroshima, Japan.

Background: Takotsubo cardiomyopathy (TCM) and neurogenic pulmonary edema (NPE) are rare complications of an acute ischemic stroke. In particular, TCM and NPE, following carotid endarterectomy (CEA) are extremely rare. In general, TCM- and NPE-associated ischemic strokes are caused by excess catecholamine release after sympathetic nervous stimulation following stroke onset, but the mechanism triggering this stimulation is still unknown. Read More

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http://dx.doi.org/10.1016/j.wneu.2018.12.206DOI Listing
January 2019
2 Reads

The cardioprotective properties and the involved mechanisms of NaoXinTong Capsule.

Pharmacol Res 2019 Jan 17;141:409-417. Epub 2019 Jan 17.

Department of Pharmacological Sciences, College of Food and Biological Engineering, Hefei University of Technology, Hefei, China. Electronic address:

NaoXinTong Capsule (NXT), a prescribed traditional Chinese medicine, is made up of 16 natural herbal materials with more than 200 identified bioactive compounds. Multiple protective effects of NXT on cardiovascular diseases including atherosclerosis, coronary artery disease, acute coronary syndrome, coronary microembolization, myocardial infarction, ischemic stroke and ischemia-reperfusion injury, have been reported by both clinical and basic studies. Biologically, these cardioprotective effects can be correlated to the actions of NXT on inflammation, apoptosis, oxidative stress, neovascularization, insulin sensitivity and lipid/glucose metabolism. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10436618183166
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http://dx.doi.org/10.1016/j.phrs.2019.01.024DOI Listing
January 2019
6 Reads

Effect of Yokukansan on Nitric Oxide Production and Hydroxyl Radical Metabolism During Cerebral Ischemia and Reperfusion in Mice.

J Stroke Cerebrovasc Dis 2019 Jan 14. Epub 2019 Jan 14.

Department of Neurology, Saitama Medical University, Moroyama, Saitama, Japan. Electronic address:

Background: The purpose of this study was to investigate the effects of yokukansan on forebrain ischemia. Because we can measure nitric oxide production and hydroxyl radical metabolism continuously, we investigated the effect of yokukansan on nitric oxide production and hydroxyl radical metabolism in cerebral ischemia and reperfusion.

Methods: Yokukansan (300 mg per kg per day) was mixed into feed and given to 8 mice for 10 days. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10523057183075
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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2018.12.047DOI Listing
January 2019
5 Reads

Hemopexin alleviates cognitive dysfunction after focal cerebral ischemia-reperfusion injury in rats.

BMC Anesthesiol 2019 Jan 15;19(1):13. Epub 2019 Jan 15.

Department of Anesthesiology, Tianjin Institute of Anesthesiology, General Hospital of Tianjin Medical University, No. 154 Anshan Road, Heping District, Tianjin, 300052, People's Republic of China.

Background: Ischemia-reperfusion (I/R) is a critical pathophysiological basis of cognitive dysfunction caused by ischemia stroke. Heme-oxygenase-1 (HO-1) is the rate-limiting enzyme for the elimination of excessive free heme by combining with hemopexin (HPX), a plasma protein that contributes to eliminating excessive free heme during ischemia stroke. This study aimed to elucidate whether HPX could alleviate cognitive dysfunction in rats subjected to cerebral I/R. Read More

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http://dx.doi.org/10.1186/s12871-019-0681-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334464PMC
January 2019
1 Read

Combined proteomic and metabolomic analyses of cerebrospinal fluid from mice with ischemic stroke reveals the effects of a Buyang Huanwu decoction in neurodegenerative disease.

PLoS One 2019 15;14(1):e0209184. Epub 2019 Jan 15.

Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.

Ischemic stroke is one of the most common causes of death worldwide and is a major cause of acquired disability in adults. However, there is still a need for an effective drug for its treatment. Buyang Huanwu decoction (BHD), a traditional Chinese medicine (TCM) prescription, has long been used clinically to aid neurological recovery after stroke. Read More

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0209184PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333407PMC
January 2019
6 Reads

Pharmacologic ATF6 activation confers global protection in widespread disease models by reprograming cellular proteostasis.

Nat Commun 2019 01 14;10(1):187. Epub 2019 Jan 14.

San Diego State University Heart Institute and the Department of Biology, San Diego State University, San Diego, CA, 92182, USA.

Pharmacologic activation of stress-responsive signaling pathways provides a promising approach for ameliorating imbalances in proteostasis associated with diverse diseases. However, this approach has not been employed in vivo. Here we show, using a mouse model of myocardial ischemia/reperfusion, that selective pharmacologic activation of the ATF6 arm of the unfolded protein response (UPR) during reperfusion, a typical clinical intervention point after myocardial infarction, transcriptionally reprograms proteostasis, ameliorates damage and preserves heart function. Read More

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http://dx.doi.org/10.1038/s41467-018-08129-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6331617PMC
January 2019

DUSP14 rescues cerebral ischemia/reperfusion (IR) injury by reducing inflammation and apoptosis via the activation of Nrf-2.

Biochem Biophys Res Commun 2019 Feb 9;509(3):713-721. Epub 2019 Jan 9.

Department of Anesthesiology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, China. Electronic address:

Ischemic stroke is the second most common cause of death, a major cause of acquired disability in adults. However, the pathogenesis that contributes to ischemic stroke has not been fully understood. Dual-specificity phosphatase 14 (DUSP14, also known as MKP6) is a MAP kinase phosphatase, playing important role in regulating various cellular processes, including oxidative stress and inflammation. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S0006291X183285
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http://dx.doi.org/10.1016/j.bbrc.2018.12.170DOI Listing
February 2019
2 Reads

Trpm2 enhances physiological bioenergetics and protects against pathological oxidative cardiac injury: Role of Pyk2 phosphorylation.

J Cell Physiol 2019 Jan 13. Epub 2019 Jan 13.

Center for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine of Temple University, Philadelphia, Pennsylvania.

The mechanisms by which Trpm2 channels enhance mitochondrial bioenergetics and protect against oxidative stress-induced cardiac injury remain unclear. Here, the role of proline-rich tyrosine kinase 2 (Pyk2) in Trpm2 signaling is explored. Activation of Trpm2 in adult myocytes with H O resulted in 10- to 21-fold increases in Pyk2 phosphorylation in wild-type (WT) myocytes which was significantly lower (~40%) in Trpm2 knockout (KO) myocytes. Read More

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http://dx.doi.org/10.1002/jcp.28146DOI Listing
January 2019
2 Reads

Nucleic Acid Therapies for Ischemic Stroke.

Neurotherapeutics 2019 Jan 11. Epub 2019 Jan 11.

Division of Neurocritical Care, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, 600 N. Wolfe Street, Baltimore, MD, 21287, USA.

Stroke remains a leading cause of disability and death worldwide despite significant scientific and therapeutic advances. Therefore, there is a critical need to improve stroke prevention and treatment. In this review, we describe several examples that leverage nucleic acid therapeutics to improve stroke care through prevention, acute treatment, and recovery. Read More

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http://dx.doi.org/10.1007/s13311-019-00710-xDOI Listing
January 2019
2 Reads

Neutrophil elastase plays a non-redundant role in remodeling the venular basement membrane and neutrophil diapedesis post ischemia/reperfusion injury.

J Pathol 2019 Jan 11. Epub 2019 Jan 11.

William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, UK.

Ischemia/reperfusion (I/R) injury is a severe inflammatory insult associated with numerous pathologies such as myocardial infarction, stroke and acute kidney injury. I/R injury is characterized by a rapid influx of activated neutrophils secreting toxic free radical species and degrading enzymes that can irreversibly damage the tissue, thus impairing organ functions. Significant efforts have been invested in identifying therapeutic targets to suppress neutrophil recruitment and activation post I/R injury. Read More

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http://dx.doi.org/10.1002/path.5234DOI Listing
January 2019
3 Reads

AP-1 (Activated Protein-1) Transcription Factor JunD Regulates Ischemia/Reperfusion Brain Damage via IL-1β (Interleukin-1β).

Stroke 2019 Feb;50(2):469-477

From the Center for Molecular Cardiology, University of Zurich, Schlieren, Switzerland (C.D.-C., M.F.R., N.R.B., L.L., P.W., H.A., S.B.-S., J.H.B., A.A., T.F.L., G.G.C.).

Background and Purpose- Inflammation is a major pathogenic component of ischemia/reperfusion brain injury, and as such, interventions aimed at inhibiting inflammatory mediators promise to be effective strategies in stroke therapy. JunD-a member of the AP-1 (activated protein-1) family of transcription factors-was recently shown to regulate inflammation by targeting IL (interleukin)-1β synthesis and macrophage activation. The purpose of the present study was to assess the role of JunD in ischemia/reperfusion-induced brain injury. Read More

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https://www.ahajournals.org/doi/10.1161/STROKEAHA.118.023739
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http://dx.doi.org/10.1161/STROKEAHA.118.023739DOI Listing
February 2019
5 Reads

IRAK-M Deficiency Exacerbates Ischemic Neurovascular Injuries in Experimental Stroke Mice.

Front Cell Neurosci 2018 21;12:504. Epub 2018 Dec 21.

Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Innate immune response to neuronal death is one of the key events of the pathogenesis of ischemic brain injury. Interleukin-1 receptor-associated kinase (IRAK)-M, encoded by gene , negatively regulates toll-like receptor signaling by interacting with the MyD88-IRAK-4-IRAK-1 complex and blocking the phosphorylation and dissociation of IRAK-1. Its function in the ischemic stroke is unknown. Read More

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https://www.frontiersin.org/article/10.3389/fncel.2018.00504
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http://dx.doi.org/10.3389/fncel.2018.00504DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6308305PMC
December 2018
5 Reads

1, 25-D Protects From Cerebral Ischemia by Maintaining BBB Permeability via PPAR-γ Activation.

Front Cell Neurosci 2018 17;12:480. Epub 2018 Dec 17.

Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

The blood-brain barrier (BBB) is a physical and biochemical barrier that maintains cerebral homeostasis. BBB dysfunction in an ischemic stroke, results in brain injury and subsequent neurological impairment. The aim of this study was to determine the possible protective effects of 1, 25-dihydroxyvitamin D [1, 25(OH)D, 1, 25-D, vit D] on BBB dysfunction, at the early stages of an acute ischemic brain injury. Read More

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https://www.frontiersin.org/article/10.3389/fncel.2018.00480
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http://dx.doi.org/10.3389/fncel.2018.00480DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304345PMC
December 2018
9 Reads

TAT-Ngn2 Enhances Cognitive Function Recovery and Regulates Caspase-Dependent and Mitochondrial Apoptotic Pathways After Experimental Stroke.

Front Cell Neurosci 2018 14;12:475. Epub 2018 Dec 14.

Department of Anesthesiology, Xiang'an Hospital, Xiamen University, Xiamen, China.

Neurogenin-2 (Ngn2) is a basic helix-loop-helix (bHLH) transcription factor that contributes to the identification and specification of neuronal fate during neurogenesis. In our previous study, we found that Ngn2 plays an important role in alleviating neuronal apoptosis, which may be viewed as an attractive candidate target for the treatment of cerebral ischemia. However, novel strategies require an understanding of the function and mechanism of Ngn2 in mature hippocampal neurons after global cerebral ischemic injury. Read More

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https://www.frontiersin.org/article/10.3389/fncel.2018.00475
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http://dx.doi.org/10.3389/fncel.2018.00475DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302814PMC
December 2018
6 Reads
4.289 Impact Factor

Metformin reduces neuronal damage and promotes neuroblast proliferation and differentiation in a cerebral ischemia/reperfusion rat model.

Neuroreport 2019 Feb;30(3):232-240

Xuzhou Key Laboratory of Neurobiology, Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Department of Cell Biology and Neurobiology, Xuzhou Medical University.

According to the previous research, metformin, a medication utilized for type 2 diabetes management, inhibits neural aging and reduces infarct size by enhancing angiogenesis in a mouse stroke model. What is more, metformin administration also promotes neural precursor cells proliferation, migration, as well as differentiation for newborn mice with hypoxia-ischemia brain injury. However, whether metformin regulates neurogenesis in an adult rat ischemia/reperfusion (I/R) model remains unclear. Read More

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http://dx.doi.org/10.1097/WNR.0000000000001190DOI Listing
February 2019

Valproic acid attenuates global cerebral ischemia/reperfusion injury in gerbils via anti-pyroptosis pathways.

Neurochem Int 2019 Mar 3;124:141-151. Epub 2019 Jan 3.

Key Laboratory of Minstry of Education for TCM Viscera State Theory and Applications, Liaoning University of Traditional Chinese Medicine, Shenyang, 110847, China. Electronic address:

Ischemic stroke is the third most common cause of death and the leading cause of disability worldwide in adults. The antiepileptic drug valproic acid (VPA) was reported to protect cerebral ischemia/reperfusion injury. However, the action mechanism of VPA in cerebral ischemia/reperfusion injury has not been fully understood. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S01970186183015
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http://dx.doi.org/10.1016/j.neuint.2019.01.003DOI Listing
March 2019
5 Reads

Mesenchymal stem cells transfer mitochondria into cerebral microvasculature and promote recovery from ischemic stroke.

Microvasc Res 2019 May 3;123:74-80. Epub 2019 Jan 3.

Department of Neurology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Mesenchymal stem cells can be used as a novel treatment of ischemic stroke, but their therapeutic effect and mechanism of action require further evaluation. Mitochondrial dysfunction has core functions in ischemia-reperfusion stroke injury. Our recent research has demonstrated that mesenchymal stem cells can transfer their functional mitochondria to injured endothelial cells via tunneling nanotubes in vitro, resulting in the rescue of aerobic respiration and protection of endothelial cells from apoptosis. Read More

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http://dx.doi.org/10.1016/j.mvr.2019.01.001DOI Listing

YiQi Tongluo Granule against cerebral ischemia/reperfusion injury in rats by freezing GluN2B and CaMKⅡ through NMDAR/ERK1/2 Signaling.

Chem Pharm Bull (Tokyo) 2018 Dec 28. Epub 2018 Dec 28.

Anhui Province Key Laboratory of Chinese Medicinal Formula, Anhui University of Chinese Medicine.

Yiqi Tongluo Granule (YQTL) is a kind of proprietary Chinese medicine, manufactured by China Shineway Pharmaceutical Group Ltd, under the authority of China Food and Drug Administration (CFDA) treating cardiovascular and cerebrovascular diseases such as ischemic stroke in China, however the underlying mechanism of YQTL on treating ischemic stroke has not been revealed. This study is aimed to evaluate the protective effect of YQTL on cerebral ischemia reperfusion (I/R) injury and inquire into its underlying mechanisms. Cerebral I/R injury was induced by occluding the middle cerebral artery for 2 h followed by 24 h reperfusion. Read More

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http://dx.doi.org/10.1248/cpb.c18-00806DOI Listing
December 2018

The Role of Macrophage Migration Inhibitory Factor in Remote Ischemic Conditioning Induced Hepatoprotection in A Rodent Model of Liver Transplantation.

Shock 2018 Dec 21. Epub 2018 Dec 21.

Department of Surgery and Transplantation, RWTH-Aachen University, Aachen, Germany.

Background: Macrophage migration inhibitory factor (MIF) is an important stress-regulating mediator of acute ischemia/reperfusion (I/R) injury and ischemic conditioning. The present study aimed to investigate whether MIF is involved in the effects of remote ischemic conditioning (RIC) in a rat model of orthotopic liver transplantation (OLT).

Methods: OLTs were performed in male Lewis rats (245-340 g). Read More

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http://dx.doi.org/10.1097/SHK.0000000000001307DOI Listing
December 2018
2 Reads

Gasdermin D serves as a key executioner of pyroptosis in experimental cerebral ischemia and reperfusion model both in vivo and in vitro.

J Neurosci Res 2019 Jan 2. Epub 2019 Jan 2.

Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.

Even though ischemic stroke is among the leading causes of death worldwide, the pathogenic mechanisms underlying ischemia reperfusion (I/R) brain injury remain unclear. Gasdermin D (GSDMD), as an important factor of pyroptotic death execution downstream of caspase-11 (noncanonical inflammasome) and caspase-1 (canonical inflammasome), may be implicated in I/R injury. The current study aimed to investigate the role and possible underlying mechanisms of GSDMD in pyroptosis during I/R injury. Read More

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http://dx.doi.org/10.1002/jnr.24385DOI Listing
January 2019
2 Reads

Upregulation of miR-496 decreases cerebral ischemia/reperfusion injury by negatively regulating BCL2L14.

Neurosci Lett 2018 Dec 28;696:197-205. Epub 2018 Dec 28.

Department of Neurology, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan 423000, PR China.

Neurological functions were seriously impaired by cerebral ischemia-reperfusion (I/R) injury following ischemic stroke and its molecular mechanism is still not fully understood. MicroRNA-496 (miR-496) has been reported to be deregulated in several diseases but it still remains unknown about the function of miR-496 in cerebral I/R injury. Here, Middle cerebral artery occlusion/reperfusion (MCAO/R) was performed to induce cerebral I/R injury in rats. Read More

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http://dx.doi.org/10.1016/j.neulet.2018.12.039DOI Listing
December 2018

NDRG4 protects against cerebral ischemia injury by inhibiting p53-mediated apoptosis.

Brain Res Bull 2019 Mar 26;146:104-111. Epub 2018 Dec 26.

Department of Neurology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China. Electronic address:

Cerebral ischemia is one of the leading causes of death and long-term disability worldwide. N-myc downstream-regulated gene 4 (NDRG4) is predominantly expressed in the brain as well as in the heart and has been reported to be involved in resistance to neuronal cell death caused by ischemic injury. However, the underlying mechanism of NDRG4 in cerebral ischemia/reperfusion (I/R) injury remains unknown. Read More

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http://dx.doi.org/10.1016/j.brainresbull.2018.12.010DOI Listing
March 2019
2 Reads
2.718 Impact Factor