Neutrophil adhesion to histamine stimulated cultured endothelial cells is primarily mediated via activation of phospholipase C and nitric oxide synthase isozymes

摘要: Objective and Design: In order to understand the underlying mechanism of histamine stimulated inflammatory responses, receptor subtypes signal transduction pathways by which mediates stimulation neutrophil adhesion endothelial cells has been studied in vitro.¶Material: Human neutrophils human umbilical vein cells.¶Treatment: Confluent cell layer were incubated with (1 mM), H1, H2 or H3 agonists: fluorophenylhistamine (10 μM), amthamine μm), methylhistamine respectively. Ten minutes prior mM) antagonists (dimethindene, 100 μM; famotidine, μM, thioperamid respectively) added. Histamine inhibited adding phospholipase C inhibitor 2-nitro-4-carboxyphenyl N,N-diphenylcarbamat (200 adenylate cyclase 9-(2 tetrahydrofuryl)adenine (80 nitric oxide synthase isozymes S-ethylisothiourea μM) guanylate (LY 83583; 10 μM). Neutrophil was monitored at 30, 60, 90, 120, 150, 180 210 min.¶Methods: quantified analysing alkaline phosphatase activity.¶Results: resulted a biphasic time concentration dependent pattern adhesion. This mimicked H1 agonists. Stimulation an agonist had no effect on binding. Inhibition (PLC), (NOS) (GC) significant decrease binding cells. An increase unstimulated observed during inhibition cyclase.¶Conclusions: Our results suggest that is due mediated activation PLC, NOS GC. Increase cAMP seems mediate inhibitory PMN