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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1103561

Received for publication November 13, 2003.
Revised January 8, 2004.
Accepted for publication January 15, 2004.

Article

Effects of cis-resveratrol on inflammatory murine macrophages: antioxidant activity and down-regulation of inflammatory genes

José Leiro *, Ezequiel Álvarez {dagger}, Juan A. Arranz *, Reyes Laguna {dagger}, Eugenio Uriarte {ddagger}, and Francisco Orallo {dagger}@

Departamentos de *Microbiología y Parasitología, {dagger}Farmacología, y {ddagger}Química Orgánica, Facultad de Farmacia, Universidad de Santiago de Compostela, Spain

@ To whom correspondence should be addressed. E-mail: fforallo{at}usc.es.


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Abstract

This study investigated for the first time the effects of the cis isomer of resveratrol (c-RESV) on the responses of inflammatory murine peritoneal macrophages, namely on the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during the respiratory burst; on the biosynthesis of other mediators of inflammation such prostaglandins; and on the expression of inflammatory genes such as inducible nitric oxide synthase (NOS)-2 and inducible cyclooxygenase (COX)-2. Treatment with 1-100 µM c-RESV significantly inhibited intracellular and extracellular ROS production, and c-RESV at 10-100 µM significantly reduced RNS production. c-RESV at 1-100 µM was ineffective for scavenging superoxide radicals (O2•-), generated enzymatically by a hypoxanthine/xanthine oxidase (XO) system and/or for inhibiting XO activity. However, c-RESV at 10-100 µM decreased nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate oxidase activity in macrophage homogenates. c-RESV at 100 µM decreased NOS-2 and COX-2 mRNA levels in lipopolysaccharide/interferon-{gamma}-treated macrophages. At 10-100 µM, c-RESV also significantly inhibited NOS-2 and COX-2 protein synthesis and decreased prostaglandin E2 (PGE2) production. These results indicate that c-RESV at micromolar concentrations significantly attenuates several components of the macrophage response to proinflammatory stimuli (notably, production of O2•- and of the proinflammatory mediators NO• and PGE2).

Key Words: NADH/NADPH oxidase • xanthine oxidase • nitric oxide • inducible nitric oxide synthase • cyclooxygenase-2 • prostaglandin E2




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