H. pylori-induced gastric mucosal injury and inflammation are mediated by proinflammatory cytokines such as interleukin

(IL)-8 and IL-1β as well as inflammatory enzymes, including inducible nitric oxide synthase (iNOS). Transcription of these inflammatory mediators is regulated by the oxidant-sensitive transcription factor NF-κB [6], [7], [8], [9] and [10]. NF-κB is an inducible transcription factor composed of p50/p65 (heterodimer) or p50 (homodimer) [11]. NF-κB is retained in the cytoplasm by binding to the inhibitory protein IκBα. Extracellular stimuli trigger rapid degradation of IκBα by proteasomes, allowing NF-κB to translocate into the nucleus and bind Enzalutamide to the DNA sites of target genes, including IL-8, IL-1β, and iNOS [12]. Therefore, degradation of IκBα represents activation of NF-κB. H. pylori-elicited neutrophils produce ROS, which subsequently injure gastric mucosal cells [13]. ROS cause peroxidation of membrane lipids, thus increasing the level of lipid peroxide (LPO) in the damaged tissues. We previously demonstrated that LPO production increases in parallel with IL-8

production in H. pylori-infected cells [7]. Myeloperoxidase (MPO) is more abundantly expressed in neutrophils than click here other cells and thus, is used as a biomarker for neutrophil infiltration [14]. In neutrophils, MPO produces hypochlorous acid from hydrogen peroxide and chloride anion during respiratory bursts. Furthermore, it oxidizes tyrosine to form tyrosyl radicals using hydrogen peroxide. Both hypochlorous acid and tyrosyl radicals

cause lipid peroxidation sequences [15]. Therefore, high levels of LPO and increased MPO activity could reflect oxidative damage and inflammatory responses of cells. Korean Red Ginseng, which is the steamed root of a 6-year-old Korean ginseng (Panax ginseng Meyer), is used in Asian countries as a traditional medicine for the treatment of various diseases, including inflammatory disorders ever [16], [17] and [18]. The most effective components of Korean Red Ginseng are triterpeneglysides known as ginsenosides [19]. Ginsenosides have anti-inflammatory [20] and [21] and anticancer effects [22]. An in vitro study showed that Korean Red Ginseng inhibited adhesion of H. pylori to gastric epithelial cells [23]. Korean Red Ginseng extract (RGE) inhibits H. pylori-induced oxidative damage in gastric epithelial cells [24] and [25]. Previously we showed hepatoprotective effects of Korean Red Ginseng in rats and mouse liver, which may be contributed by its antioxidant activity [26] and [27]. Therefore, the antioxidant or anti-inflammatory effects of RGE, containing ginsenosides, may protect gastric mucosa from inflammation caused by H. pylori infection. In the present study, we investigated whether RGE protects against H. pylori-induced gastric inflammation in Mongolian gerbils. Animal models for H.