Figures & data
Figure 1. H. pylori-induced oxidative stress in stomach. LPS: lipopolysaccharide; NAP: neutrophil-activating protein; PMN: polymorphonuclear neutrophil; CagA: cytotoxin-associated gene A; PGN: peptidoglycan; MPO: myeloperoxidase; H2O2: hydrogen peroxide; NH2Cl: monocloramine; OCl−: hypochlorite ion; NADP+/NADPH: nicotinamide adenine dinucleotide phosphate/reduced form of NADP+.
Figure 2. Factors in H. pylori-induced gastric inflammation. cagPAI: cag pathogenicity island; VacA: vacuolating cytotoxin A; PicA: permit the induction of cytokines A; PicB: permit the induction of cytokines B; Tipα: tumor necrosis factorα inducing protein; SabA: sialic acid-binding adhesin A; CsrA: carbon storage regulator A; AhpC: alkyl hydroperoxide reductase C; Tpx: thiol-peroxidases; KatA: catalase A; SodB: superoxide dismutase B; fur: ferric uptake regulator; HSP: heat shock protein; MAPK: mitogen-activated protein kinase; MMP: matrix metalloproteinase; Shh: sonic hedgehog; IL-8: interleukin-8; IL-17: interleukin-17; iNOS: inducible nitric oxide synthase; NO: nitric oxide; TRX: thioredoxin; COX-1: cyclooxygenase-1; NADPH: nicotinamide adenine dinucleotide phosphate; Mox1: mitogen oxidase 1; 8OHdG: 8-hydroxy deoxyguanosine; SOD: superoxide dismutase; TBARS: thiobarbituric acid reactive substances; TNFα: tumor necrosis factor alpha; ROS: reactive oxygen species; NFκB: nuclear factor kappa B; CagA: cytotoxim associated gene A; NapA: neutrophil-activating protein A; Lps: lipopolysacharide; COX1: cyclokxygenare; NH2Cl: monochloradine; ROS: reactive oxygen species; H2P2: hydrogen peroxide; OCl−: hypochloride ion.
