ReviewInflammopharmacology2005
Oxidative stress in Helicobacter pylori-induced gastric cell injury.
Review in Inflammopharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Enhancement of Gastric Mucosal Defense by Phytomedicine in the Context ofBiologics : targets & therapy · 2026Review
- Metformin Inhibits the Development of Helicobacter pylori-Associated Gastritis by Regulating the ERK-MMP10-IL-1β Axis.Cell biochemistry and biophysics · 2025Article
- A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation.Heliyon · 2023Article
- Astaxanthin Inhibits Matrix Metalloproteinase Expression by Suppressing PI3K/AKT/mTOR Activation inNutrients · 2022Article
- Article
- β-Carotene Inhibits Expression of Matrix Metalloproteinase-10 and Invasion inMolecules (Basel, Switzerland) · 2021Article
- Article
- α-Lipoic Acid Inhibits Expression of IL-8 by Suppressing Activation of MAPK, Jak/Stat, and NF-κB in H. pylori-Infected Gastric Epithelial AGS Cells.Yonsei medical journal · 2016Article
- Aegle marmelos fruit extract attenuates Helicobacter pylori Lipopolysaccharide induced oxidative stress in Sprague Dawley rats.BMC complementary and alternative medicine · 2015Article
- The phenyl-thiophenyl propenone RK-I-123 reduces the levels of reactive oxygen species and suppresses the activation of NF-κB and AP-1 and IL-8 expression in Helicobacter pylori-infected gastric epithelial AGS cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- Honey: a novel antioxidant.Molecules (Basel, Switzerland) · 2012Review
- Potent antioxidant and genoprotective effects of boeravinone G, a rotenoid isolated from Boerhaavia diffusa.PloS one · 2011Article
- Role of protease-activated receptor-2 on cell death and DNA fragmentation in Helicobacter pylori-infected gastric epithelial cells.Journal of translational medicine · 2010Article
- Difference in the regulation of IL-8 expression induced by uropathogenic E. coli between two kinds of urinary tract epithelial cells.Journal of biomedical science · 2009Article
- Characterization of a Helicobacter hepaticus putA mutant strain in host colonization and oxidative stress.Infection and immunity · 2008Article
- Effects of quercetin on hyper-proliferation of gastric mucosal cells in rats treated with chronic oral ethanol through the reactive oxygen species-nitric oxide pathway.World journal of gastroenterology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.