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Published online before print February 24, 2004
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,1
Departamentos de
* Microbiología y Parasitología,
Farmacología, y
Química Orgánica, Facultad de Farmacia, Universidad de Santiago de Compostela, Spain
1Correspondence: Departamento de Farmacología, Facultad de Farmacia, Universidad de Santiago de Compostela, Campus Universitario Sur, E-15782 Santiago de Compostela (La Coruña), Spain. E-mail: fforallo{at}usc.es
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 (HX)/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 (NADH/NADPH) oxidase activity in macrophage homogenates. c-RESV at 100 µM decreased NOS-2 and COX-2 mRNA levels in lipopolysaccharide (LPS) interferon gamma (IFN-
)-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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