scholarly journals The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury

2013 ◽  
Vol 34 (3) ◽  
pp. 480-488 ◽  
Author(s):  
Beatriz Rodriguez-Grande ◽  
Matimba Swana ◽  
Loan Nguyen ◽  
Pavlos Englezou ◽  
Samaneh Maysami ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Edema ◽  
Acute Phase ◽  
Acute Phase Protein ◽  
Ischemic Injury ◽  
Glial Scar ◽  
Scar Formation ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Phase Protein

Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effects on acute ischemic brain injury. In contrast, the absence of PTX3 strongly compromised blood–brain barrier integrity and resolution of brain edema during recovery after ischemic injury. Compromised resolution of brain edema in PTX3-deficient mice was associated with impaired glial scar formation and alterations in scar-associated extracellular matrix production. Our results suggest that PTX3 expression induced by proinflammatory signals after ischemic brain injury is a critical effector of edema resolution and glial scar formation. This highlights the potential role for inflammatory molecules in brain recovery after injury and identifies APPs, in particular PTX3, as important targets in ischemic stroke and possibly other brain inflammatory disorders.

scholarly journals Effect of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats

2018 ◽  
Vol 17 (1) ◽  
pp. 69-73
Author(s):  
N. S. Shcherbak ◽  
M. A. Popovetskiy ◽  
G. Yu. Yukina ◽  
M. M. Galagudza
Keyword(s):  
Brain Injury ◽  
Acute Phase ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Single Application ◽  
Ischemic Brain

Curcumin presents antioxidant and anti-inflammatory properties and can be considered as a neuroprotector. Data on doses and duration of application of curcumin to achieve protective effects in various types of ischemic brain injury is controversial. The purpose was to study the neuroprotective properties of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats. It is shown that a single application of curcumin (300 mg/kg, i.p.) is not has neuroprotective effect in the acute phase of ischemia in chronic hypoperfusion in Wistar rats. The results allow to conclude that the neuroprotective effect of a single application of curcumin.

Dextrorphan Reduces Infarct Volume, Vascular Injury, and Brain Edema after Ischemic Brain Injury

1996 ◽  
Vol 13 (4) ◽  
pp. 215-222 ◽  
Author(s):  
CHENG DU ◽  
RONG HU ◽  
CHUNG Y. HSU ◽  
DENNIS W. CHOI
Keyword(s):  
Brain Injury ◽  
Brain Edema ◽  
Vascular Injury ◽  
Infarct Volume ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

CINC‐1 is identified as an acute‐phase protein induced by focal brain injury causing leukocyte mobilization and liver injury

2003 ◽  
Vol 17 (9) ◽  
pp. 1168-1170 ◽  
Author(s):  
Sandra J. Campbell ◽  
Paula M. Hughes ◽  
John P. Iredale ◽  
David C. Wilcockson ◽  
Sara Waters ◽  
...  
Keyword(s):  
Brain Injury ◽  
Liver Injury ◽  
Acute Phase ◽  
Acute Phase Protein ◽  
Leukocyte Mobilization ◽  
Phase Protein ◽  
Focal Brain Injury

scholarly journals Toll-Like Receptor 9: A New Target of Ischemic Preconditioning in the Brain

2008 ◽  
Vol 28 (5) ◽  
pp. 1040-1047 ◽  
Author(s):  
Susan L Stevens ◽  
Thomas MP Ciesielski ◽  
Brenda J Marsh ◽  
Tao Yang ◽  
Delfina S Homen ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Injury ◽  
Ischemic Brain Injury ◽  
Dependent Manner ◽  
Cpg Odn ◽  
Toll Like Receptor ◽  
Ischemic Brain ◽  
Cpg Oligodeoxynucleotide ◽  
Tlr9 Ligand

Preconditioning with lipopolysaccharide (LPS), a toll-like receptor 4 (TLR4) ligand, provides neuroprotection against subsequent cerebral ischemic brain injury, through a tumor necrosis factor (TNF)α-dependent process. Here, we report the first evidence that another TLR, TLR9, can induce neuroprotection. We show that the TLR9 ligand CpG oligodeoxynucleotide (ODN) can serve as a potent preconditioning stimulus and provide protection against ischemic brain injury. Our studies show that systemic administration of CpG ODN 1826 in advance of brain ischemia (middle cerebral artery occlusion (MCAO)) reduces ischemic damage up to 60% in a dose- and time-dependent manner. We also offer evidence that CpG ODN preconditioning can provide direct protection to cells of the central nervous system, as we have found marked neuroprotection in modeled ischemia in vitro. Finally, we show that CpG preconditioning significantly increases serum TNFα levels before MCAO and that TNFα is required for subsequent reduction in damage, as mice lacking TNFα are not protected against ischemic injury by CpG preconditioning. Our studies show that preconditioning with a TLR9 ligand induces neuroprotection against ischemic injury through a mechanism that shares common elements with LPS preconditioning via TLR4.

scholarly journals Immunomodulation with Human Umbilical Cord Blood Stem Cells Ameliorates Ischemic Brain Injury – A Brain Transcriptome Profiling Analysis

2019 ◽  
Vol 28 (7) ◽  
pp. 864-873 ◽  
Author(s):  
Maple L. Shiao ◽  
Ce Yuan ◽  
Andrew T. Crane ◽  
Joseph P. Voth ◽  
Mario Juliano ◽  
...  
Keyword(s):  
Stem Cells ◽  
Brain Injury ◽  
Umbilical Cord Blood ◽  
Ischemic Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Brain Transcriptome ◽  
Blood Stem Cells ◽  
Cord Blood Stem Cells ◽  
The Brain

Our group previously demonstrated that administration of a CD34-negative fraction of human non- hematopoietic umbilical cord blood stem cells (UCBSC) 48 h after ischemic injury could reduce infarct volume by 50% as well as significantly ameliorate neurological deficits. In the present study, we explored possible mechanisms of action using next generation RNA sequencing to analyze the brain transcriptome profiles in rats with ischemic brain injury following UCBSC therapy. Two days after ischemic injury, rats were treated with UCBSC. Five days after administration, total brain mRNA was then extracted for RNAseq analysis using Illumina Hiseq 2000. We found 275 genes that were significantly differentially expressed after ischemic injury compared with control brains. Following UCBSC treatment, 220 of the 275 differentially expressed genes returned to normal levels. Detailed analysis of these altered transcripts revealed that the vast majority were associated with activation of the immune system following cerebral ischemia which were normalized following UCBSC therapy. Major alterations in gene expression profiles after ischemia include blood-brain-barrier breakdown, cytokine production, and immune cell infiltration. These results suggest that UCBSC protect the brain following ischemic injury by down regulating the aberrant activation of innate and adaptive immune responses.

scholarly journals Ischemic Brain Injury Leads to Brain Edema via Hyperthermia-Induced TRPV4 Activation

2018 ◽  
Vol 38 (25) ◽  
pp. 5700-5709 ◽  
Author(s):  
Yutaka Hoshi ◽  
Kohki Okabe ◽  
Koji Shibasaki ◽  
Takashi Funatsu ◽  
Norio Matsuki ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Edema ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

scholarly journals Electroacupuncture increased cerebral blood flow and reduced ischemic brain injury: dependence on stimulation intensity and frequency

2011 ◽  
Vol 111 (6) ◽  
pp. 1877-1887 ◽  
Author(s):  
Fei Zhou ◽  
Jingchun Guo ◽  
Jieshi Cheng ◽  
Gencheng Wu ◽  
Ying Xia
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Stimulation Parameters ◽  
Cerebral Artery Occlusion ◽  
The Brain

Stroke causes ischemic brain injury and is a leading cause of neurological disability and death. There is, however, no promising therapy to protect the brain from ischemic stress to date. Here we show an exciting finding that optimal electroacupuncture (EA) effectively protects the brain from ischemic injury. The experiments were performed on rats subjected to middle cerebral artery occlusion (MCAO) with continuous monitoring of cerebral blood flow. EA was delivered to acupoints of “Shuigou” (Du 26) and “Baihui” (Du 20) with different intensities and frequencies to optimize the stimulation parameters. The results showed that 1) EA at 1.0–1.2 mA and 5–20 Hz remarkably reduced ischemic infarction, neurological deficit, and death rate; 2) the EA treatment increased the blood flow by >100%, which appeared immediately after the initiation of EA and disappeared after the cessation of EA; 3) the EA treatment promoted the recovery of the blood flow after MCAO; 4) “nonoptimal” parameters of EA (e.g., <0.6 mA or >40 Hz) could not improve the blood flow or reduce ischemic injury; and 5) the same EA treatment with optimal parameters could not increase the blood flow in naive brains. These novel observations suggest that appropriate EA treatment protects the brain from cerebral ischemia by increasing blood flow to the ischemic brain region via a rapid regulation. Our findings have far-reaching impacts on the prevention and treatment of ischemic encephalopathy, and the optimized EA parameters may potentially be a useful clue for the clinical application of EA.

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