Laminin peptide ameliorates brain injury by inhibiting leukocyte accumulation in a rat model of transient focal cerebral ischemia

Kiyoyuki Yanaka, Paul J. Camarata, Stephen R. Spellman, Amy P Skubitz, Leo T Furcht, Walter C Low

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26 Scopus citations

Abstract

Postischemic cerebral inflammation has been reported to contribute to ischemic brain damage. During inflammation, constituents of the extracellular matrix such as fibronectin and laminin are recognized by certain integrins or proteoglycans and play an important role in the cell adhesion process. The purpose of this study was to evaluate the efficacy of peptides derived from laminin on leukocyte accumulation, infarct size, and neurological outcome in rats subjected to 1 h of cerebral ischemia and 48 h of reperfusion. Forty- four animals were included in this study: transient ischemia without treatment (Group I), treatment with TG-1 peptide (Group II), GD-I peptide (Group III), and GD-6 peptide (Group IV). Group II showed a significant reduction of the leukocyte accumulation (p < 0.001) and infarct size (p = 0.015) when compared with Group I. The neurological grade of Group II was also significantly better than in Group I at 48 h after reperfusion (p = 0.012). Based on these data, which are the first to explore the therapeutic potential of this peptide in cerebral ischemia, laminin peptide may offer a novel therapeutic approach to allaying injury in ischemic stroke.

Original languageEnglish (US)
Pages (from-to)605-611
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Volume17
Issue number6
DOIs
StatePublished - Jun 1997

Keywords

  • Adhesion molecules
  • Cerebral ischemia
  • Laminin
  • Leukocytes
  • Reperfusion

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