Search our Database of Scientific Publications and Authors

I’m looking for a

    Details and Download Full Text PDF:
    The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord.

    Neuroscience 2006 Jul 3;140(3):1011-22. Epub 2006 Apr 3.
    Spinal Cord Injury Team, Laboratory of Spinal Cord Injury, BioTherapeutics Research Group, Robarts Research Institute, 100 Perth Drive, London, Ontario, Canada N6A 5K8.
    The tripeptide, phenylalanine-glutamate-glycine (FEG) and its d-isomeric form phenylalanine-(D) glutamate-(D) glycine (feG), derived from submandibular gland peptide-T, significantly reduce the allergic inflammatory response and leukocyte trafficking and neutrophil migration into intestine, heart and lungs. Due to these actions, we hypothesized that feG would attenuate the early inflammatory response to spinal cord injury, reduce free radical production and improve neurological outcomes, like other leukocyte-limiting strategies we have used previously. We tested this using a clip compression model of spinal cord injury in rats. Following spinal cord injury at the 4th thoracic cord segment, we quantified leukocyte infiltration, free radical formation and oxidative damage at the lesion site after feG or control peptide phenylalanine-(D) aspartate-(D) glycine treatment. In rats treated with feG at 2 and 12 h, or 6 and 12 h after spinal cord injury, mean myeloperoxidase activity and ED-1 expression were significantly lower ( approximately 40%) than in controls at 24 h. Free radical formation generated in injured spinal cord was detected using 2',7'-dichlorofluorescin-diacetate as a fluorescent probe. Free radical production in the injured cord increased significantly after spinal cord injury and feG treatment significantly reduced this free radical production. Oxidative enzymes, lipid peroxidation and cell death were also significantly ( approximately 40%), gp91 ( approximately 30%), thiobarbituric acid reactive substance levels ( approximately 35%), 4-hydroxynonenal-bound protein ( approximately 35%) and caspase-3 ( approximately 32%). Early administration of feG decreases infiltration of inflammatory cells into the injured spinal cord and intraspinal free radical formation, thereby reducing oxidative damage and secondary cell death after spinal cord injury.
    PDF Download - Full Text Link
    ( Please be advised that this article is hosted on an external website not affiliated with PubFacts.com)
    Source Status
    http://dx.doi.org/10.1016/j.neuroscience.2006.02.061DOI ListingPossible

    Similar Publications

    Effects of a novel tripeptide on neurological outcomes after spinal cord injury.
    Neuroreport 2006 Nov;17(17):1793-6
    Spinal Cord Injury Team, BioTherapeutics Research Group, Robarts Research Institute, London, Ontario, Canada.
    A biologically active tripeptide [phenylalanine glutamate glycine (feG)] derived from the submandibular gland has anti-inflammatory actions. We have shown that intravenous treatment with feG after spinal cord injury decreases the intraspinal infiltration of leukocytes and associated oxidative damage within 72 h after injury. The present study assessed effects of this treatment on chronic neurological outcomes after clip-compression spinal cord injury at the 12th thoracic segment. Read More
    Effectiveness of FK506 on lipid peroxidation in the spinal cord following experimental traumatic injury.
    Spinal Cord 2005 Jan;43(1):22-6
    Department of Neurosurgery, Gazi University Medical School, Beşevler, Ankara, Turkey.
    Study Design: An in vivo study in Wistar albino rats with injured spinal cord.

    Setting: Department of Neurosurgery, Biochemistry and Pathology, Gazi University, Ankara, Turkey.

    Objectives: The aim of this study was to investigate and compare the effects of FK506 an immunosupressive agent with methylprednisolone (MP) on lipid peroxidation (LP) in injured spinal cord tissue. Read More
    Early anti-inflammatory treatment reduces lipid peroxidation and protein nitration after spinal cord injury in rats.
    J Neurochem 2004 Mar;88(6):1335-44
    Spinal Cord Injury Team, BioTherapeutics Research Group, Robarts Research Institute, London, Ontario, Canada.
    We investigated mechanisms by which a monoclonal antibody (mAb) against the CD11d subunit of the leukocyte integrin CD11d/CD18 improves neurological recovery after spinal cord injury (SCI) in the rat. The effects of an anti-CD11d mAb treatment were assessed on ED-1 expression (estimating macrophage infiltration), myeloperoxidase activity (MPO, approximating neutrophil infiltration), lipid peroxidation, inducible nitric oxide synthase (iNOS) and nitrotyrosine (indicating protein nitration) expression in the spinal cord lesion after severe clip-compression injury. Protein expression was evaluated by western blotting and immunocytochemistry. Read More
    An integrin inhibiting molecule decreases oxidative damage and improves neurological function after spinal cord injury.
    Exp Neurol 2008 Dec 26;214(2):160-7. Epub 2008 Sep 26.
    Spinal Cord Injury Laboratory, BioTherapeutics Research Group, Robarts Research Institute, Schulich School of Medicine and Dentistry, The University of Western Ontario, PO Box 5015, 100 Perth Drive, London, Ontario Canada.
    Our previous studies have shown that treatment with an alpha4beta1 integrin blocking antibody after spinal cord injury (SCI) in rats decreases intraspinal inflammation and oxidative damage, improving neurological function. Here, we studied effects of a high affinity small molecule alpha4beta1 inhibitor, BIO5192. First, rats were treated intravenously with BIO5192 (10 mg/kg) or with vehicle (controls) to assess effects of integrin blockade for 24 h or 72 h after thoracic clip-compression SCI. Read More