In Vitro Evidence of the Role of COX-2 in Attenuating Gastric Inflammation and Promoting Gastric Carcinogenesis

Hahm, Ki‐Baik; Lim, Ho-Yeong; Sohn, Seonghyang; Kwon, Hyuk‐Jae; Lee, Ki-Myung; Lee, Jeong-Sang; Surh, Young‐Joon; Kim, Young‐Bae; Joo, Hee-Jae; Kim, Won‐Seok; Cho, Seung-Won

doi:10.1615/jenvironpatholtoxicoloncol.v21.i2.100

Cited by 17 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The 8-OHdG content of patients whose H. pylori was eradicated was significantly decreased after 2 weeks of eradication medications (Table 1). We also found suppression of transforming growth factor-b1 expression directly in the gastric epithelium, which enables unlimited oxidative bursts in recruited macrophages by H. pylori infection (19).…”

Section: Reversibility Of Oxidative Dna Damage By Eradication Of H Pmentioning

confidence: 58%

“…2) (29). Interestingly, increased DNA binding of NF-kB after H. pylori injection could be decreased after the administration of the antioxidative and antiinflammatory drug, rebamipide (1,15,19,21). Therefore, H. pylori provoked gastric inflammation through several cytokines, whose expression is controlled by gene transcriptional factors such as NF-kB or AP-1.…”

Section: Gastric Inflammation Induced By H Pylorimentioning

confidence: 99%

See 1 more Smart Citation

Amelioration of Oxidative Stress with Ensuing Inflammation Contributes to Chemoprevention ofH. pylori-Associated Gastric Carcinogenesis

Park

Kim²,

Choi³

et al. 2004

Antioxidants & Redox Signaling

Self Cite

View full text Add to dashboard Cite

The gastric inflammatory response provoked by Helicobacter pylori (H. pylori) consists of infiltrations by neutrophils, lymphocytes, and macrophages, resulting in varying degrees of epithelial cell damage. H. pylori-associated inflammation not only activates various oxidant-producing enzymes such as NADPH oxidase and inducible nitric oxide synthase, but also lowers the antioxidant ascorbic acid in the stomach. Reactive oxygen metabolites and nitrogen metabolites generated by these enzymes react with each other to generate new or more potent reactive species. The specific types of cellular damage resulting from reactive oxygen metabolites include lipid peroxidation, protein oxidation, and oxidative DNA damage. All of these oxidative products can result in biochemical changes leading to cancer. A positive association has been demonstrated between H. pylori infection and gastric adenocarcinoma with increased oxidative stress. Therefore, appropriate treatment to reduce oxidative stress would be expected to prevent subsequent gastric carcinogenesis through lessening of H. pylori-associated inflammation. This review will provide evidence that antiinflammatory regimens can decrease the development of tumors and the amelioration of gastric inflammation might lead to chemoprevention strategies by the attenuation of oxidative stress.

show abstract

Section: Reversibility Of Oxidative Dna Damage By Eradication Of H Pmentioning

confidence: 58%

Section: Gastric Inflammation Induced By H Pylorimentioning

confidence: 99%

Amelioration of Oxidative Stress with Ensuing Inflammation Contributes to Chemoprevention ofH. pylori-Associated Gastric Carcinogenesis

Park

Kim²,

Choi³

et al. 2004

Antioxidants & Redox Signaling

Self Cite

View full text Add to dashboard Cite

show abstract

“…Accordingly, H. pylori-induced inflammatory responses potentially have positive functions in resisting certain cancer-advancement-related biological processes post the development of GC and showing better outlook in those patients, although they have played fundamental roles during the phase of cancer formation. Interestingly, the COX-2 expression induced by H. pylori still seems to be able to attenuate the degree of AG, the initial event of GC, though it plays a role in gastric carcinogenesis (Hahm et al, 2002). COX-2-dependent PGE2 also shows a protective effect during the oncogenic process of Hp-GC in that it can prevent H. pylori-induced gastric preneoplasia and reverse preexisting lesions by suppressing IFN-expression (Toller et al, 2010).…”

Section: Beneficial Edge Of the Swordmentioning

confidence: 99%

A Double-Edged Sword: Roles of Helicobacter Pylori in Gastric Carcinoma

Xue¹,

Su²,

Mao³

et al. 2011

Gastric Carcinoma - Molecular Aspects and Current Advances

View full text Add to dashboard Cite

“…Expression of inflammatory genes, such as iNOS, is primarily controlled by the transcriptional regulation. The promotor of iNOS gene has nuclear factor‐kappaB (NF‐κB)‐binding sites, and H. pylori is known to stimulate activation of NF‐κB 9,10 . In resting cells, hetero‐ or homodimer of Rel protein family comprises NF‐κB that is normally sequestered in the cytoplasm as an inactive complex with an inhibitory subunit IκBα.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effects of 7‐Carboxymethyloxy‐3′,4′,5‐Trimethoxy Flavone (DA‐6034) on Helicobacter pylori‐Induced NF‐κB Activation and iNOS Expression in AGS Cells

Lee

Kim

Hahm

et al. 2007

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

The Helicobacter pylori were identified by Marshall and Warren in 1984. H. pylori survive in the forbidding harsh acid environment of the stomach and duodenum by hiding in the mucus layer and neutralizing gastric acid in its local surrounding environment. Multiple lines of evidence suggest that H. pylori infection is one of the primary causes of gastritis and peptic ulcer, which are provoked by oxidative stress and inflammation. More than 50% of the world's population is infected by this bacterium. The H. pylori-induced inflammation has been implicated in the pathogenesis and progression of gastric cancer. DA-6034 (7-carboxymethyloxy-3',4',5-trimethoxy flavone) is a synthetic flavonoid known to possess anti-inflammatory activity. It has been reported that oral administration of DA-6034 suppresses the inflammatory bowel disease (IBD) in animal models. In this article, we attempted to examine the effect of DA-6034 on H. pylori-induced inflammation in human gastric cancer (AGS) cells by targeting NF-kappaB and extracellular signal-regulated kinase (ERK), a representative MAPK.

show abstract

In Vitro Evidence of the Role of COX-2 in Attenuating Gastric Inflammation and Promoting Gastric Carcinogenesis

Cited by 17 publications

References 0 publications

Amelioration of Oxidative Stress with Ensuing Inflammation Contributes to Chemoprevention ofH. pylori-Associated Gastric Carcinogenesis

Amelioration of Oxidative Stress with Ensuing Inflammation Contributes to Chemoprevention ofH. pylori-Associated Gastric Carcinogenesis

A Double-Edged Sword: Roles of Helicobacter Pylori in Gastric Carcinoma

Inhibitory Effects of 7‐Carboxymethyloxy‐3′,4′,5‐Trimethoxy Flavone (DA‐6034) on Helicobacter pylori‐Induced NF‐κB Activation and iNOS Expression in AGS Cells

Contact Info

Product

Resources

About