Inhibition by magnolol of formylmethionyl-leucyl-phenyl alanine-induced respiratory burst in rat neutrophils

J Pharm Pharmacol. 1999 Mar;51(3):285-94. doi: 10.1211/0022357991772466.


The influence of the plant product magnolol on neutrophil superoxide anion (O2-*) generation has been investigated in the rat. Intraperitoneal injection of magnolol (30mg kg(-1)) significantly inhibited the formylmethionyl-leucyl-phenylalanine (fMLP)-induced respiratory burst in rat whole blood ex-vivo. Magnolol also inhibited the 02-* generation with an IC50 (concentration resulting in 50% inhibition) of 15.4+/-1.6 microM and O2 consumption in rat neutrophils in-vitro. Magnolol weakly inhibited the O2-* 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 microM and the phosphorylation of mitogen-activated protein kinase p42/44 with an IC50 of 28.5+/-4.5 microM. However, magnolol alone activated neutrophil phospholipase D activity as determined by the formation of phosphatidic acid and phosphatidyl-ethanol 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Biphenyl Compounds / pharmacology*
  • Blotting, Western
  • Cyclic AMP / metabolism
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cyclic GMP / metabolism
  • Drug Interactions
  • Lignans*
  • Luminescent Measurements
  • Mitogens / pharmacology
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology*
  • Neutrophils / drug effects*
  • Oxygen / metabolism
  • Phospholipase D / metabolism
  • Phosphorylation / drug effects
  • Protein Kinase C / metabolism
  • Rats
  • Respiratory Burst / drug effects*
  • Superoxides / metabolism*
  • Xanthine Oxidase / physiology


  • Anti-Inflammatory Agents, Non-Steroidal
  • Biphenyl Compounds
  • Lignans
  • Mitogens
  • magnolol
  • Superoxides
  • N-Formylmethionine Leucyl-Phenylalanine
  • Cyclic AMP
  • Xanthine Oxidase
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Phospholipase D
  • Cyclic GMP
  • Oxygen