The influence of the plant product magnolol on neutrophil superoxide anion (O-2(-.)) generation has been investigated in the rat. Intraperitoneal injection of magnolol (30 mg kg(-1)) significantly inhibited the formyl-methionyl-leucyl-phenylalanine (fMLP)-induced respiratory burst in rat whole blood exvivo. Magnolol also inhibited the O-2(-.) generation with an IC50 (concentration resulting in 50% inhibition) of 15.4+/-1.6 mu M and O-2 consumption in rat neutrophils in-vitro. Magnolol weakly inhibited the O-2(-.) generation in the xanthine-xanthine oxidase system, decreased cellular cyclic AMP level and had no effect on cyclic GMP levels. It weakly inhibited neutrophil cytosolic protein kinase C activity but did not alter porcine heart protein kinase A activity. Magnolol attenuated fMLP-induced protein tyrosine phosphorylation with an IC50 of 24.0+/-1.9 mu M and the phosphorylation of mitogen-activated protein kinase p42/44 with an IC50 of 28.5+/-4.5 mu M. However, magnolol alone activated neutrophil phospholipase D activity as determined by the formation of phosphatidic acid and phosphatidylethanol in the presence of ethanol. In the presence of NADPH, the arachidonate-activated NADPH oxidase activity in a cell-free system was weakly suppressed by magnolol. These results suggest that the inhibition of respiratory burst in fMLP-activated neutrophils by magnolol is probably attributable mainly to the attenuation of protein tyrosine phosphorylation and p42/44 mitogen-activated protein kinase activation, and partly to the suppression of protein kinase C and NADPH oxidase activities.
關聯:
AMERICAN JOURNAL OF CHINESE MEDICINE 27(1):123-128
