Kim Hyeyoung
Department of Pharmacology and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, South Korea.
Inflammopharmacology. 2005;13(1-3):63-74. doi: 10.1163/156856005774423962.
Oxygen radicals are supposed to be involved in inflammation and cell proliferation. Helicobacter pylori induces decrease in antioxidant defense factors, such as GSH, mucus and constitutive nitric oxide (NO), gastric mucosal injury and inflammation. Inflammation and injury might be caused by oxidant-mediated expression of inflammatory cytokine interleukin-8 (IL-8) and inflammatory enzymes such as cyclooxtgenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were mediated by oxidant-sensitive transcription factors such as nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), possibly with mitogen activated protein kinase (MAPK) activation. H. pylori-induced alterations in protein expression demonstrate the involvement of oxidative stress in the pathogenesis of H. pylori-induced gastric diseases. The differentially expressed genes and proteins may be useful as prognostic indices for gastric diseases associated with H. pylori infection. In conclusion, oxygen radicals are produced in gastric epithelial cells infected with H. pylori, which may reduce the antioxidant defense mechanism and turn on the expression of inflammatory genes, adhesion molecules and mediators stimulating cell proliferation, as well as defensive molecular chaperones in gastric epithelial cells.
氧自由基被认为与炎症和细胞增殖有关。幽门螺杆菌会导致抗氧化防御因子如谷胱甘肽（GSH）、黏液和组成型一氧化氮（NO）减少，引发胃黏膜损伤和炎症。炎症和损伤可能是由氧化剂介导的炎性细胞因子白细胞介素-8（IL-8）以及炎性酶如环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的表达所致，这些是由对氧化剂敏感的转录因子如核因子-κB（NF-κB）和激活蛋白-1（AP-1）介导的，可能伴有丝裂原活化蛋白激酶（MAPK）的激活。幽门螺杆菌诱导的蛋白质表达改变表明氧化应激参与了幽门螺杆菌所致胃部疾病的发病机制。差异表达的基因和蛋白质可能作为与幽门螺杆菌感染相关胃部疾病的预后指标。总之，在感染幽门螺杆菌的胃上皮细胞中会产生氧自由基，这可能会降低抗氧化防御机制，并开启炎性基因、黏附分子以及刺激细胞增殖的介质的表达，还有胃上皮细胞中的防御性分子伴侣的表达。
