ANTIINFLAMMATORY EFFECT OF MAGNOLOL, ISOLATED FROM MAGNOLIA OFFICINALIS, ON A23187-INDUCED PLEURISY IN MICE

In the present study, A23187-induced pleurisy in mice was used to investigate the anti-inflammatory effect of magnolol, a phenolic compound isolated from Chinese medicine Hou p'u (cortex of Magnolia officinalis. A23187-induced protein leakage was reduced by magnolol (10 mg kg(-1), i.p.), indomethacin (10 mg kg(-1), i.p.) and BW755C (30 mg kg(-1), i.p.). A23187-induced polymorphonuclear (PMN) leucocyte infiltration in the pleural cavity was suppressed by magnolol and BW755C, while enhanced by indomethacin. Like BW755C, magnolol reduced both prostaglandin E(2) (PGE(2)) and leukotriene B-4 (LTB(4)) levels in the pleural fluid of A23187-induced pleurisy, while indomethacin reduced PGE(2) but increased LTB(4) formation. In the rat isolated peripheral neutrophil suspension, magnolol (3.7 mu M) and BW755C (10 mu M) also suppressed the A23187-induced thromboxane B-2 (TXB(2)) and LTB(4) formation. These results suggest that magnolol, like BW755C, might be a dual cyclo-oxygenase and lipoxygenase inhibitor. The inhibitory effect of magnolol on the A23187-induced pleurisy is proposed to be, at least partly, dependent on the reduction of the formation of eicosanoids mediators in the inflammatory site.