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Thread: Uric Acid May Help Reduce Effects of Spinal Cord Injury, Jefferson Researchers Find

  1. #1
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    Uric Acid May Help Reduce Effects of Spinal Cord Injury, Jefferson Researchers Find

    Uric Acid May Help Reduce Effects of Spinal Cord Injury, Jefferson Researchers Find
    PHILADELPHIA, Feb. 14 (AScribe Newswire) -- Increasing levels of uric acid, a metabolic breakdown product found in blood and urine, may help cut some of the potentially devastating "secondary" cellular damage that occurs following a spinal cord injury, say researchers at Jefferson Medical College. The finding may lead to new treatments for such injuries.

    After a spinal cord injury, the body's inflammatory response may actually make things worse, releasing a variety of potentially harmful chemicals that can make the injury more severe. J. Craig Hooper, Ph.D., associate professor of microbiology and immunology at Jefferson Medical College of Thomas Jefferson University in Philadelphia and at Jefferson's Kimmel Cancer Center and his colleagues there and at the University of Messina in Italy looked at whether uric acid treatment could actually prevent some of this secondary damage following such an injury in mice. Uric acid was known to reduce inflammation damage related to a compound called peroxynitrite.

    They found that mice that received uric acid just before and right after an experimental spinal cord injury recovered motor function both faster and to a greater extent than mice that received only saline. Subsequent tests found that the uric acid actually prevented inflammation and some damage. Tests in cell culture showed that uric acid protected spinal cord neurons from peroxynitrite-related damage. The scientists report their findings Feb. 14, 2005, in the Proceedings of the National Academy of Sciences.

    According to Dr. Hooper, secondary spinal cord damage -- the so-called destructive cascade -- begins within a few hours after the initial injury. "The effect is driven by nonspecific cells such as neutrophils," he explains, a type of white blood cell and a key player in the body's inflammatory response to injury. "We know neutrophils make peroxynitrite, which is a major trigger in opening the blood-brain barrier."

    Dr. Hooper says peroxynitrite is known to contribute to cell damage in neurodegenerative disorders, and is known to be produced as a result of the body's i
    http://www.ascribe.org/cgi-bin/behol...=2005&public=1



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    Compound in Urine May Fight Spinal Cord Injury

    Compound in Urine May Fight Spinal Cord Injury
    -- Robert Preidt


    TUESDAY, Feb. 15 (HealthDay News) -- Uric acid, a metabolic breakdown product found in urine and blood, may help reduce damage from spinal cord injury, researchers say.

    In research with mice, scientists at Thomas Jefferson University, Philadelphia, found that uric acid helped lessen some of the secondary cellular damage that occurs following spinal cord injury. This secondary damage is caused when the body's inflammatory response releases potentially harmful chemicals that exacerbate the injury.

    Mice given uric acid just before and after they suffered a spinal cord injury recovered motor function quicker, and to a greater degree, than mice receiving a simple saline solution. In cell culture tests, the researchers discovered that uric acid protected spinal cord neurons from damage caused by a compound called peroxynitrite, which is linked to cell damage caused by inflammation.

    http://www.forbes.com/lifestyle/heal...out523944.html



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  3. #3
    Interesting. This reminds me of that old article about tauroursodeoxycholic acid from bile being neuroprotective. Wonder if the compounds are related.

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    Senior Member Max's Avatar
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    Uric acid may help reduce effects of spinal cord injury

    Uric acid may help reduce effects of spinal cord injury



    Increasing levels of uric acid, a metabolic breakdown product found in blood and urine, may help cut some of the potentially devastating "secondary" cellular damage that occurs following a spinal cord injury, say researchers at Jefferson Medical College. The finding may lead to new treatments for such injuries.

    After a spinal cord injury, the body's inflammatory response may actually make things worse, releasing a variety of potentially harmful chemicals that can make the injury more severe. J. Craig Hooper, Ph.D., associate professor of microbiology and immunology at Jefferson Medical College of Thomas Jefferson University in Philadelphia and at Jefferson's Kimmel Cancer Center and his colleagues there and at the University of Messina in Italy looked at whether uric acid treatment could actually prevent some of this secondary damage following such an injury in mice. Uric acid was known to reduce inflammation damage related to a compound call peroxynitrite.
    They found that mice that received uric acid just before and right after an experimental spinal cord injury recovered motor function both faster and to a greater extent than mice that received only saline. Subsequent tests found that the uric acid actually prevented inflammation and some damage. Tests in cell culture showed that uric acid protected spinal cord neurons from peroxynitrite-related damage. The scientists report their findings Feb. 14, 2005 in the Proceedings of the National Academy of Sciences.

    According to Dr. Hooper, secondary spinal cord damage - the so-called destructive cascade - begins within a few hours after the initial injury. "The effect is driven by nonspecific cells such as neutrophils," he explains, a type of white blood cell and a key player in the body's inflammatory response to injury. "We know neutrophils make peroxynitrite, which is a major trigger in opening the blood-brain barrier."


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    Senior Member Max's Avatar
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    Uric Acid May Help Reduce Effects Of Spinal Cord Injury, Jefferson Researchers Find

    Uric Acid May Help Reduce Effects Of Spinal Cord Injury, Jefferson Researchers Find
    Increasing levels of uric acid, a metabolic breakdown product found in blood and urine, may help cut some of the potentially devastating "secondary" cellular damage that occurs following a spinal cord injury, say researchers at Jefferson Medical College. The finding may lead to new treatments for such injuries.

    http://www.sciencedaily.com/releases...0218132721.htm



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  6. #6
    This is the abstract of the original journal article:

    Scott GS, Cuzzocrea S, Genovese T, Koprowski H and Hooper DC (2005). Uric acid protects against secondary damage after spinal cord injury. Proc Natl Acad Sci U S A 102: 3483-8. Peroxynitrite contributes to the pathogenesis of various neurodegenerative disorders through multiple mechanisms and is thought to mediate secondary neuronal cell death after spinal cord injury (SCI). Here we establish that physiologically relevant levels of uric acid (UA), a selective inhibitor of certain peroxynitrite-mediated reactions, block the toxic effects of peroxynitrite on primary spinal cord neurons in vitro. Furthermore, administration of UA at the onset of SCI in a mouse model inhibits several pathological changes in the spinal cord including general tissue damage, nitrotyrosine formation, lipid peroxidation, activation of poly(ADP-ribose) polymerase, and neutrophil invasion. More importantly, UA treatment improves functional recovery from the injury. Taken together, our findings support the concept that peroxynitrite contributes to the pathophysiology of secondary damage after SCI. They also raise the possibility that elevating UA levels may provide a therapeutic approach for the treatment of SCI as well as other neurological diseases with a peroxynitrite-mediated pathological component. Department of Microbiology and Immunology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107.

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    Uric acid and spinal cord injury treatment

    Uric acid and spinal cord injury treatment

    A novel approach from Rutgers holds potential for central nervous system damage

    NEW BRUNSWICK/PISCATAWAY, N.J. -- Uric acid is commonly associated with the excruciatingly painful joint disease known as gout, but it can also play a crucial role in the treatment of spinal cord injury and other central nervous system disorders, such as stroke, multiple sclerosis and Parkinson's disease, according to Rutgers' Bonnie Firestein.
    Firestein, an associate professor of cell biology and neuroscience at Rutgers, The State University of New Jersey, and her laboratory team have reported their discovery in the Early View (online in advance of print) version of the journal Glia.
    "In spinal cord injury, as well as stroke, two kinds of damage can occur," Firestein explained. "First there is the physical damage, but this is followed by secondary chemical damage to neurons [nerve cells] by compounds released in response to the trauma. We have found that uric acid can promote an early intervention step in combating this chemical damage through its action on astroglial cells."
    Astroglial cells or astrocytes are specialized cells that support neuron function with nutrients and protective buffering.
    In addition to the scientific achievement, the research study is a model for student involvement and education. Among the co-authors, postdoctoral associate Yangzhou Du is teaching Firestein more about astroglial cells, while he is learning about neurons from her. Christopher Chen was a Henry Rutgers Honors undergraduate student on the study, and Yuval Eisenberg, a laboratory technician; both now attend medical school. Another student, Chia-Yi Tseng is continuing her graduate studies in Firestein's laboratory.
    Uric acid's effects on the health of neurons had been observed by other researchers, but the mechanics of how it confers protection has remained a mystery.
    "It is interesting to note that people with gout never seem to develop multiple sclerosis," Firestein said. "In animal models of multiple sclerosis, the addition of uric acid reduces symptoms and improves prognosis. The same is true for one type of Parkinson's disease tested."
    The Firestein team's breakthrough studies revealed that uric acid can stimulate astroglial cells to produce transporter proteins that carry harmful compounds away from neurons in jeopardy of chemical damage. This opens the door to identifying a unique drug target for new therapies.

    http://www.eurekalert.org/pub_releas...-uaa010307.php

  8. #8
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    Tnx Max. This quote in your link is interesting;

    When Firestein's group added uric acid to a mixed culture of rat spinal cord neurons and astroglial cells, the production of the glutamate transporter EAAT-1 increased markedly. The challenge now is find the most effective strategy for increasing the production of the transporter, using drug therapies or other means.

    Firestein said that a collaborative team of colleagues from Baylor College of Medicine and the University of Rochester Medical Center has devised one such strategy. With this team, Firestein will develop a line of stem cells that has been modified to generate astrocytes that produce large quantities of the EAAT-1 transporter. Adding these to an injury site, either alone or in combination with uric acid, holds great potential, she said.
    What is this, has it anything to do with this?
    The research team led by Stephen Davies from Baylor College of Medicine, Houston, USA and colleagues from the University of Rochester Medical Center, New York, USA took embryonic glial precursor cells and induced them to differentiate in culture into a specific type of embryonic astrocyte known to be highly supportive of nerve fibre growth. They hoped these cells would have the repair capabilities of the embryonic spinal cord, which is lost in adults. Davies et al. transplanted these cells into cuts in the spinal cord of adult rats and measured the growth of nerve fibres by labelling them with a dye. They then compared healing and recovery in these rats with the recovery in spinal cord injured rats that received either undifferentiated glial precursor cells or no treatment at all.
    Source.
    Anyone?

  9. #9
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    Schmeky or DA (you'r in the Baylor neighborhood), maybe you have heard someting?

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