TNF was used as a stimulating factor to study the effects of glucocorticoid (GC) on poly-morphonuclear leucocyte (PMN) adhesion. The results showed that tumor necrosis factor (TNF) could increase the PMN adhesion markedly, and Dex could not inhibit the PMN adhesion induced by TNF, but it had a certain effect of prevention. PMN adhesion was increased prominently when Dex and RU 38486 were given after TNF pretreatment. The received results testify to ability of propranolol to increase adhesion and modulation of apoptosis and PMN free oxygen radicals production. The drugs' effect on PMN free oxygen radicals production, apoptosis and adhesion may constitute an additional mechanism of their activity. However, thus there was a stimulation of monokines production - TNF-α and IL-1. Introduction of obsidan to immunized mice as well as dihydroergotamine enhanced production of TNF-б and reduced production of IL-2.
TNF was used as a stimulating factor to study the effects of glucocorticoid (GC) on poly-morphonuclear leucocyte (PMN) adhesion. The results showed that tumor necrosis factor (TNF) could increase the PMN adhesion markedly, and Dex could not inhibit the PMN adhesion induced by TNF, but it had a certain effect of prevention. PMN adhesion was increased prominently when Dex and RU 38486 were given after TNF pretreatment. The received results testify to ability of propranolol to increase adhesion and modulation of apoptosis and PMN free oxygen radicals production. The drugs' effect on PMN free oxygen radicals production, apoptosis and adhesion may constitute an additional mechanism of their activity. However, thus there was a stimulation of monokines production - TNF-α and IL-1. Introduction of obsidan to immunized mice as well as dihydroergotamine enhanced production of TNF-б and reduced production of IL-2.