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      [6]-Gingerol inhibits nitric oxide synthesis in activated J774.1 mouse macrophages and prevents peroxynitrite-induced oxidation and nitration reactions.

      Life Sciences

      Macrophage Activation, Catechols, Cells, Cultured, DNA Damage, drug effects, Dose-Response Relationship, Drug, Enzyme Induction, Fatty Alcohols, pharmacology, Fluoresceins, metabolism, Ginger, Lipopolysaccharides, Animals, physiology, Macrophages, enzymology, Mice, Nitric Oxide, biosynthesis, Nitric Oxide Synthase, antagonists & inhibitors, Nitric Oxide Synthase Type II, Oxidation-Reduction, Peroxynitrous Acid

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          Abstract

          Reactive nitrogen species (RNS), such as nitric oxide (NO) and its derivatives, e.g. peroxynitrite (ONOO-), have been proposed as being able to influence signal transduction and cause DNA damage, contributing to carcinogenic processes. In this study, the effect of [6]-gingerol, a pungent phenolic compound present in ginger (Zingiber officinale Roscoe), on NO synthesis in lipopolysaccharide (LPS)-activated J774.1 macrophages was tested, and the protective ability of this compound against peroxynitrite-mediated oxidation and nitration reactions were evaluated. [6]-Gingerol exhibited dose-dependent inhibition of NO production and significant reduction of inducible NO synthase (iNOS) in LPS-stimulated J774.1 cells. Moreover, [6]-gingerol effectively suppressed peroxynitrite-induced oxidation of dichlorodihydrofluorescein, oxidative single strand breaks in supercoiled pTZ 18U plasmid DNA, and formation of 3-nitrotyrosine in bovine serum albumin (BSA) and J774.1 cells. Our results indicate that [6]-gingerol is a potent inhibitor of NO synthesis and also an effective protector against peroxynitrite-mediated damage.

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          14572883

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