Abstract
In a trial to investigate whether phospholipase inhibition hypothesis is the sole interpretation of mechanism underlying anti-inflammatory action of glucocorticoids, the present experiments were undertaken to determine whether the steroids directly inhibit inflammatory action of a variety of cyclo-oxygenase and lipoxygenase products and to determine whether there is a difference in the mode of anti-inflammatory action between the steroid and inhibitors to cyclo-oxygenase and lipoxygenase. Vasodilator effect of E-type prostaglandin (PG) in microcirculation of inflammatory tissue was determined by measuring the blood content of the tissue with the aid of radiochromium-labeled red blood cells. Vascular permeability responses induced with PGE and a combination of PGE with bradykinin were measured on the responses of swelling of the footpad of mice. Plasma exudation in the rat skin induced with leukotriene (LT) C and D and a combination of LTC with PGE was measured with the aid of radioiodine-labeled serum albumin. All of these inflammatory responses provoked by the application of the lipoxygenase and cyclo-oxygenase products were effectually prevented by pre-treatment of animals with glucocorticoid. Anti-exudative effects of glucocorticoids were compared with those of lipoxygenase and cyclo-oxygenase inhibitor BW755C by using carrageenin-air-pouch inflammation in rats. BW755C was effective in inhibiting plasma exudation only in the acute stage of the inflammation similarly as in cases of indomethacin, aspirin, phenylbutazone and naproxen, whereas glucocorticoids were effective in both the acute and chronic stages. The steroids are considered to inhibit generation of PGs and LTs through induction of a phospholipase-inhibitory protein, macrocortin or lipomodulin. However, the present study indicates that anti-inflammatory effects of the steroid should be attributed rather to its more direct anti-inflammatory action other than inhibition of phospholipase.
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