Suppression of inflammatory cell recruitment by histamine receptor stimulation in ischemic rat brains

摘要: Abstract Inflammation is a crucial factor in the development of ischemia-induced brain injury. Since facilitation central histaminergic activity ameliorates reperfusion injury, effects postischemic administration l -histidine, precursor histamine, and thioperamide, histamine H3 receptor antagonist, on inflammatory cell infiltration were evaluated rat model transient occlusion middle cerebral artery. After for 12, 24, or 72 h following 2 h occlusion, slices immunohistochemically stained with antibodies against myeloperoxidase CD68, which markers polymorphonuclear leukocytes macrophages/microglia, respectively. 12–24 h, number neutrophils ischemic side increased markedly, whereas increase was not observed contralateral side. Administration -histidine (1000 mg/kg × 2, i.p.), immediately 6 h after reperfusion, reduced to 52%. Simultaneous thioperamide (5 mg/kg, s.c.) further decreased 32%. Likewise, ischemia induced CD68-positive cells 24 h suppressed by injections. The CD4+T lymphocytes both sides 12 h, concurrent prolonged effect. Although mepyramine (3 nmol, i.c.v.) did affect suppression leukocyte infiltration, ranitidine tended reverse effect -histidine. These data suggest that enhancement suppresses recruitment events through H2 receptors, may be mechanism underlying protective