Suppression of inflammatory cell recruitment by histamine receptor stimulation in ischemic rat brains
| Autor: | Tatsuru Arai, Naoto Adachi, Takumi Nagaro, Norihito Hiraga, Keyue Liu |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
CD4-Positive T-Lymphocytes
Male Time Factors Neutrophils Cell Count Pharmacology Ranitidine Brain Ischemia Brain ischemia Random Allocation chemistry.chemical_compound Histamine receptor Piperidines Histamine H2 receptor Antigens CD Animals Medicine Histidine Rats Wistar Peroxidase Pyrilamine Thioperamide business.industry Histaminergic Infarction Middle Cerebral Artery medicine.disease Immunohistochemistry Rats Drug Combinations Histamine H2 Antagonists chemistry Reperfusion Immunology Histamine H1 Antagonists Receptors Histamine Histamine H3 receptor business Reperfusion injury Histamine medicine.drug |
| Zdroj: | European Journal of Pharmacology. 557:236-244 |
| ISSN: | 0014-2999 |
| DOI: | 10.1016/j.ejphar.2006.11.020 |
| Popis: | Inflammation is a crucial factor in the development of ischemia-induced brain injury. Since facilitation of central histaminergic activity ameliorates reperfusion injury, effects of postischemic administration of l -histidine, a precursor of histamine, and thioperamide, a histamine H3 receptor antagonist, on inflammatory cell infiltration were evaluated in a rat model of transient occlusion of the middle cerebral artery. After reperfusion for 12, 24, or 72 h following 2 h of occlusion, brain slices were immunohistochemically stained with antibodies against myeloperoxidase and CD68, which were markers of polymorphonuclear leukocytes and macrophages/microglia, respectively. After reperfusion for 12–24 h, the number of neutrophils on the ischemic side increased markedly, whereas the increase was not observed on the contralateral side. Administration of l -histidine (1000 mg/kg × 2, i.p.), immediately and 6 h after reperfusion, reduced the number of neutrophils to 52%. Simultaneous administration of thioperamide (5 mg/kg, s.c.) further decreased the number of neutrophils to 32%. Likewise, the ischemia induced increase in the number of CD68-positive cells after 24 h was suppressed by l -histidine injections. The l -histidine administration decreased the number of CD4+T lymphocytes on both ischemic and contralateral sides after 12 h, and concurrent administration of thioperamide prolonged the effect. Although administration of mepyramine (3 nmol, i.c.v.) did not affect suppression of leukocyte infiltration, ranitidine tended to reverse the effect of l -histidine. These data suggest that enhancement of central histaminergic activity suppresses inflammatory cell recruitment after ischemic events through histamine H2 receptors, which may be a mechanism underlying the protective effect of l -histidine. |
| Databáze: | OpenAIRE |
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