Indomethacin enhanced macrophage cytostasis against MOPC-315 tumor cells in vitro. The effect of indomethacin was inhibited by prostaglandin E2 and by the lipoxygenase inhibitor nordihydroguaiaretic acid. Prostaglandin E2 and nordihydroguaiaretic acid also inhibited indomethacin stimulation of macrophage thymidine incorporation. Indomethacin inhibited macrophage prostaglandin E2 formation and stimulated leukotriene B4 synthesis. Nordihydroguaiaretic acid inhibited leukotriene B4 production. Our data indicate that eicosanoids play a role in regulating macrophage cytostasis.
On the basis of previous findings it was suggested that estriol-16,17-dihemisuccinate might counteract the development of induced local oedemas. To test this assumption, a study was performed using the rat paw oedema test. Depending on the material used, three types of oedema could be produced:
Rapid and transient type, when serotonin, histamine, compound 48/80, chicken egg white and polyvinylpyrrolidone were the inducers. Slow and long lasting type, with kaolin as inducer. Rapid and long lasting type when cobra venom served as inducer.
Cyproheptadine inhibited the rapid and transient type of oedema, except when polyvinylpyrrolidone was used. Furthermore cyproheptadine counteracted the rapid phase of the oedema produced by cobro venom, but did not influence the slow and long lasting oedema induced by kaolin or the delayed phase of the cobra venom oedema.
Phenylbutazone counteracted the slow and long lasting swelling induced by kaolin and the delayed phase of swelling induced by the snake venom, but exerted no effect on any rapid and transient oedema, or on the early phase of oedema produced by snake venom.
Estriol-16,17-dihemisuccinate did not selectively inhibit any one kind of oedema more than another, but counteracted at approximately equal potency all the types of oedema studied.
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