Suppression of <i>Helicobacter pylori</i>‐induced interleukin‐8 production in gastric cancer cell lines by an anti‐ulcer drug, geranylgeranylacetone

Yoshimura, Naoki; Suzuki, Yasuo; Saitō, Yasushi

doi:10.1046/j.1440-1746.2002.02880.x

Cited by 9 publications

(6 citation statements)

References 35 publications

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“…It is thought that treatment with GGA suppresses the increase in neutrophil accumulation in the colons of mice with TNBS-induced colitis. Recently, it has been reported that GGA regulates the expression of interleukin-8 in the gastric mucosa (34,35). Although the mechanism by which GGA suppressed neutrophil accumulation in colon tissue from mice with TNBS-induced colitis was not clarified in the present study, previous studies and the present study suggest that GGA inhibits neutrophil accumulation via mediating the expressions of chemokines in the colon.…”

Section: Discussioncontrasting

confidence: 54%

Protective effect of geranylgeranylacetone on trinitrobenzene sulfonic acid-induced colitis in mice

Ohkawara¹,

Nishihira²,

Takeda³

et al. 2006

Int J Mol Med

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Geranylgeranylacetone (GGA) has recently been reported to have a protective effect against ischemic, injurious and apoptotic stress in several tissues. The aim of this study was to determine the effect of GGA on colitis induced by 2,4,6trinitrobenzene sulfonic acid (TNBS) in mice. Colitis was induced by intrarectal instillation of TNBS in 50% ethanol in BALB/c mice. Survival, change in body weight and change in wet colon weight were assessed. Histological score in the colon was evaluated 5 days after TNBS treatment. The level of myeloperoxidase (MPO) activity in the colon was also determined. Immunohistochemistry for CD4 in the colon was performed. In addition, the level of heat shock protein (HSP) 70 in the colon was determined by Western blot analysis. Mice were orally treated with GGA (300 mg/kg) 2 h before and every other day after starting TNBS administration. Treatment with GGA markedly improved the survival rate, and reduced the loss of body weight and loss of wet colon weight in mice with TNBS-induced colitis. GGA also suppressed the increase in MPO activity and the number of CD4-positive cells infiltrating the colons of mice with TNBSinduced colitis. Furthermore, treatment with GGA remarkably up-regulated the expression of HSP70 in the colons of mice with TNBS-induced colitis. Our results provide further evidence that GGA has therapeutic potential for intestinal inflammation.Abbreviations: HSP, heat shock protein; GGA, geranylgeranylacetone; TNBS, trinitrobenzene sulfonic acid; MPO, myeloperoxidase; IBD, inflammatory bowel disease

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Section: Discussioncontrasting

confidence: 54%

Protective effect of geranylgeranylacetone on trinitrobenzene sulfonic acid-induced colitis in mice

Ohkawara¹,

Nishihira²,

Takeda³

et al. 2006

Int J Mol Med

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“…We therefore speculated that the decrease of H. pylori colonization density produced by teprenone in the corpus might be accounted for by other mechanisms. Recently, Yoshimura et al have also reported that teprenone at 0.1 mmol/l inhibits IL-8 mRNA expression in H. pylori-infected gastric mucosal cells (KATOIII cells) up to approximately 50% [29]. In fact, it has been shown that IL-8 levels correlate with H. pylori density and intensity of neutrophil infiltration in the gastric mucosa [28].…”

Section: Discussionmentioning

confidence: 97%

“…The inhibition rate was up to approximately 50% for 0.05 mmol/l teprenone. Recently, Yoshimura et al have also reported that teprenone at 0.1 mmol/l inhibits IL-8 mRNA expression in H. pylori-infected gastric mucosal cells (KATOIII cells) up to approximately 50% [29]. Based on our in vitro findings for teprenone, it is likely that orally administered teprenone actually inhibits IL-8 production in the gastric mucosa, because it has been confirmed that therapeutic oral doses of teprenone will reach 0.01-0.1 mmol / l in the mucosa [30].…”

Section: Discussionmentioning

confidence: 98%

Teprenone, but not H2‐Receptor Blocker or Sucralfate, Suppresses Corpus Helicobacter pylori Colonization and Gastritis in Humans: Teprenone Inhibition of H. pylori‐Induced Interleukin‐8 in MKN28 Gastric Epithelial Cell Lines

Miyake¹,

Tsukui

Shinji

et al. 2004

Helicobacter

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“…Highly expressed levels of IL-8 mRNA and protein were found in gastric cancer cells [8], [9]. It has recently been suggested that IL-8 is closely related to the tumorigenesis, angiogenesis, adhesion, invasion or metastasis of cancer [10]–[14].…”

Section: Introductionmentioning

confidence: 99%

A Meta-Analysis of Interleukin-8 -251 Promoter Polymorphism Associated with Gastric Cancer Risk

Han

et al. 2012

PLoS ONE

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BackgroundPotential functional allele A/T single nucleotide polymorphism (SNP) of Interleukin 8 (IL-8) promoter -251has been implicated in gastric cancer risk.MethodsWe aimed to explore the role of A/T SNP of IL-8 -251 in the susceptibility to gastric cancer through a systematic review and meta-analysis. Each initially included article was scored for quality appraisal. Desirable data were extracted and registered into databases. Eighteen studies were ultimately eligible for the meta-analysis of IL-8 - 251 A/T SNP. We adopted the most probably appropriate genetic model (codominant model). Potential sources of heterogeneity were sought out via stratification and sensitivity analyses, and publication biases were estimated.ResultsBetween IL-8 -251 AA genotype with gastric cancer risk, statistically significant association could be noted with overall gastric cancer, evidently noted in Asians, witnessed in high quality subgroup, and apparently noted in intestinal-type gastric cancer.ConclusionsOur meta-analysis indicates that IL-8 -251 AA genotype is associated with the overall risk of developing gastric cancer and may seem to be more susceptible to overall gastric cancer in Asian populations. IL-8 -251 AA genotype is more associated with the intestinal-type gastric cancer. IL-8 -251 AA genotype is not associated with Helicobacter Pylori infection status in our meta-analysis.ImpactThe analyses suggest that IL-8 -251 AA genotype may be an important biomarker of gastric cancer susceptibility for Asians, especially for Chinese Han population, the assumption that needs to be further confirmed in future well-designed studies in China.

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Suppression of Helicobacter pylori‐induced interleukin‐8 production in gastric cancer cell lines by an anti‐ulcer drug, geranylgeranylacetone

Cited by 9 publications

References 35 publications

Protective effect of geranylgeranylacetone on trinitrobenzene sulfonic acid-induced colitis in mice

Protective effect of geranylgeranylacetone on trinitrobenzene sulfonic acid-induced colitis in mice

Teprenone, but not H2‐Receptor Blocker or Sucralfate, Suppresses Corpus Helicobacter pylori Colonization and Gastritis in Humans: Teprenone Inhibition of H. pylori‐Induced Interleukin‐8 in MKN28 Gastric Epithelial Cell Lines

A Meta-Analysis of Interleukin-8 -251 Promoter Polymorphism Associated with Gastric Cancer Risk

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