Effect of stobadine on human stimulated polymorphonuclear leukocytes.
The effect of stobadine (0.1-100 microM) on human polymorphonuclear (PMN) leukocytes stimulated with N-formyl-methionyl-leucyl-phenylalanine, a specific receptor activator, or with the calcium ionophore, A-23187 (receptor bypassing stimulus) was investigated with respect to: i) superoxide generation, ii) beta-glucuronidase release and iii) 3[H]-arachidonic acid liberation. Stobadine was found to exert an inhibitory effect on N-formyl-methionyl-leucyl-phenylalanine but not on A-23187-stimulated PMN leukocytes. The effect was more intensive on superoxide generation and beta-glucuronidase release than on 3[H]-arachidonic acid liberation. These results indicate that the inhibitory effect of stobadine is most probably via a mechanism dependent on signal transduction across the plasma membrane. This effect may occur through inhibition of arachidonate signal transduction through a regulatory G-protein.
D000975:Antioxidants / Q000494:pharmacology*; D016718:Arachidonic Acid / Q000037:antagonists & inhibitors / Q000378:metabolism; D000001:Calcimycin / Q000494:pharmacology; D002243:Carbolines / Q000494:pharmacology*; D005966:Glucuronidase / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D007476:Ionophores / Q000494:pharmacology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D013268:Stimulation, Chemical; D013481:Superoxides / Q000037:antagonists & inhibitors / Q000378:metabolism