K. Yanaka et al., LAMININ PEPTIDE AMELIORATES BRAIN INJURY BY INHIBITING LEUKOCYTE ACCUMULATION IN A RAT MODEL OF TRANSIENT FOCAL CEREBRAL-ISCHEMIA, Journal of cerebral blood flow and metabolism, 17(6), 1997, pp. 605-611
Postischemic cerebral inflammation has been reported to contribute to
ischemic brain damage. During inflammation, constituents of the extrac
ellular matrix such as fibronectin and laminin are recognized by certa
in integrins or proteoglycans and play an important role in the cell a
dhesion process. The purpose of this study was to evaluate the efficac
y of peptides derived from laminin on leukocyte accumulation, infarct
size, and neurological outcome in rats subjected to 1 h of cerebral is
chemia and 48 h of reperfusion. Forty-four animals were included in th
is study: transient ischemia without treatment (Group I), treatment wi
th TG-1 peptide (Group II), GD-1 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 wi
th Group I. The neurological grade of Group LI 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 nove
l therapeutic approach to allaying injury in ischemic stroke.