NDLI: Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Please wait, while we are loading the content...

Tissue Plasminogen Activator Induced Delayed Edema in Experimental Porcine Intracranial Hemorrhage: Reduction with Plasminogen Activator Inhibitor-1 Administration

Interaction Between Sex and Apolipoprotein E Genetic Background in a Murine Model of Intracerebral Hemorrhage

TOMM40 in Cerebral Amyloid Angiopathy Related Intracerebral Hemorrhage: Comparative Genetic Analysis with Alzheimer’s Disease

Hyperglycemia and Outcome in Intracerebral Hemorrhage: from Bedside to Bench—More Study Is Needed

Neuregulin-1 Effects on Endothelial and Blood–Brain Barrier Permeability After Experimental Injury

Gr1+ Macrophages and Dendritic Cells Dominate the Inflammatory Infiltrate 12 h After Experimental Intracerebral Hemorrhage

Depletion of GR-1-Positive Cells Is Associated with Reduced Neutrophil Inflammation and Astrocyte Reactivity after Experimental Intracerebral Hemorrhage

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Ferumoxytol-Enhanced MRI to Image Inflammation Within Human Brain Arteriovenous Malformations: a Pilot Investigation

Micro-Computed Tomography for Hemorrhage Disruption of Mouse Brain Vasculature

Ischemic Preconditioning Attenuates Brain Edema After Experimental Intracerebral Hemorrhage

Translational Stroke Research : Volume 3, Issue 2, June 2012

Translational Stroke Research : Volume 3, Issue 1, March 2012

Translational Stroke Research : Volume 2

Translational Stroke Research : Volume 1

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Content Provider	Springer Nature Link
Author	Simard, J. Marc Tosun, Cigdem Ivanova, Svetlana Kurland, David B. Hong, Caron Radecki, Leanne Gisriel, Carter Mehta, Rupal Schreibman, David Gerzanich, Volodymyr
Copyright Year	2012
Abstract	Subarachnoid hemorrhage (SAH) can lead to disabling motor, cognitive, and neuropsychological abnormalities. Part of the secondary injury to cerebral tissues associated with SAH is attributable to the neuroinflammatory response induced by blood. Heparin is a pleiotropic compound that reduces inflammatory responses in conditions outside the central nervous system. Using a model of SAH devoid of global insult, we evaluated the effect of delayed intravenous (IV) infusion of heparin, at a dose that does not produce therapeutic anticoagulation, on neuroinflammation, myelin preservation, and apoptosis. Adult male rats underwent bilateral stereotactic injections of autologous blood (50 μL) into the subarachnoid space of the entorhinal cortex. The rats were implanted with mini-osmotic pumps that delivered either vehicle or unfractionated heparin (10 U/kg/h IV) beginning 12 h after SAH. No mechanical or hemorrhagic injury was observed in the hippocampus. In vehicle controls assessed at 48 h, SAH was associated with robust neuroinflammation in the adjacent cortex [neutrophils, activated phagocytic microglia, nuclear factor-kappa B, tumor necrosis factor-alpha, and interleukin-1beta] and neurodegeneration (Fluoro-Jade C staining and loss of NeuN). In the hippocampus, a muted neuroinflammatory response was indicated by Iba1-positive, ED1-negative microglia exhibiting an activated morphology. The perforant pathway showed Fluoro-Jade C staining and demyelination, and granule cells of the dentate gyrus had pyknotic nuclei, labeled with Fluoro-Jade C and showed upregulation of cleaved caspase-3, consistent with transsynaptic apoptosis. Administration of heparin significantly reduced neuroinflammation, demyelination, and transsynaptic apoptosis. We conclude that delayed IV infusion of low-dose unfractionated heparin may attenuate adverse neuroinflammatory effects of SAH.
Starting Page	155
Ending Page	165
Page Count	11
File Format	PDF
ISSN	18684483
Journal	Translational Stroke Research
Volume Number	3
Issue Number	1
e-ISSN	1868601X
Language	English
Publisher	Springer-Verlag
Publisher Date	2012-04-14
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Subarachnoid hemorrhage Neuroinflammation Microglia Heparin Transsynaptic apoptosis Rat Neurosurgery Cardiology Vascular Surgery Neurosciences Neurology
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine Neuroscience Neurology (clinical)

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Tenascin-C Causes Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats

PCMT1 Ameliorates Neuronal Apoptosis by Inhibiting the Activation of MST1 after Subarachnoid Hemorrhage in Rats

Rat Endovascular Perforation Model

Intravascular Inflammation Triggers Intracerebral Activated Microglia and Contributes to Secondary Brain Injury After Experimental Subarachnoid Hemorrhage (eSAH)

Cellular Microparticles in Subarachnoid Hemorrhage

The Single and Double Blood Injection Rabbit Subarachnoid Hemorrhage Model

Deferoxamine Reduces Neuronal Death and Hematoma Lysis After Intracerebral Hemorrhage in Aged Rats

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Similar Documents

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage

Tenascin-C Causes Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats

PCMT1 Ameliorates Neuronal Apoptosis by Inhibiting the Activation of MST1 after Subarachnoid Hemorrhage in Rats

Rat Endovascular Perforation Model

Intravascular Inflammation Triggers Intracerebral Activated Microglia and Contributes to Secondary Brain Injury After Experimental Subarachnoid Hemorrhage (eSAH)

Cellular Microparticles in Subarachnoid Hemorrhage

The Single and Double Blood Injection Rabbit Subarachnoid Hemorrhage Model

Deferoxamine Reduces Neuronal Death and Hematoma Lysis After Intracerebral Hemorrhage in Aged Rats

Heparin Reduces Neuroinflammation and Transsynaptic Neuronal Apoptosis in a Model of Subarachnoid Hemorrhage