A proton pump inhibitor, E3810, has an antibacterial activity through binding to Helicobacter pylori

Hirai, Masamichi; T, Azuma; Ito, Shigeji; Kato, Takaro; Kohli, Y.; Kuriyama, Masato

doi:10.1016/0016-5085(95)23118-8

Cited by 24 publications

(36 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[97,[101][102][103][104][105][106][107] Thus, the MIC range against H. pylori for rabeprazole is considerably lower than that previously reported for omeprazole or lansoprazole. [97,[101][102][103][104][105][106][107][108] Furthermore, in vitro, rabeprazole inhibits H. pylori motility [105,106] and urease activity. [109,110] However, but for some exceptions, rabeprazole monotherapy has not been able to eradicate H. pylori infection.…”

Section: Rabeprazolementioning

confidence: 99%

Potent Gastric Acid Inhibition in Helicobacter pylori Eradication

Gisbert

2005

Drugs

View full text Add to dashboard Cite

At present, antisecretory drugs -foremost among them the proton pump inhibitors (PPIs) -represent a keystone in Helicobacter pylori eradication therapy. The present article shall first compare the role of PPIs as compared with histamine H 2 receptor antagonists, both of them in the role of antibiotic-associated antisecretory therapy, and shall then address the contribution of each of the various PPIs that have been developed until the present time to the H. pylori eradication therapies. In summary, it may be concluded that PPIs are more effective overall than H 2 receptor antagonists when the two groups of antisecretory drugs are given at the usual standard doses together with antibiotics with the intention of eradicating H. pylori infection. However, all PPIs (omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole) are equivalent when given together with two antibiotics to cure the infection.

show abstract

Section: Rabeprazolementioning

confidence: 99%

Potent Gastric Acid Inhibition in Helicobacter pylori Eradication

Gisbert

2005

Drugs

View full text Add to dashboard Cite

show abstract

“…9 Rabeprazole and its primary thioether metabolite (secreted by gastric mucosal cells) have also been reported to show antimicrobial activity for H. pylori. 10,11 In the face of the above-mentioned problems with current PPI-based triple therapies in Japan, the results of small-scale studies indicate that regimens using rabeprazole can be expected to achieve more reliable eradication than regimens based on older PPIs. However, a multicentre, randomized, double-blind, large-scale study has not yet conducted in Japan.…”

Section: Introductionmentioning

confidence: 99%

Rabeprazole‐based eradication therapy for Helicobacter pylori: a large‐scale study in Japan

Kuwayama

Asaka

Sugiyama

et al. 2007

Aliment Pharmacol Ther

View full text Add to dashboard Cite

show abstract

“…Appropriately high pH values increase antimicrobial susceptibility of H pylori because the minimum inhibitory concentration of most antibiotics against H pylori is very dependent on the pH of the environment. [21][22][23][24][25][26] Previously, we found that PPIs could exercise selective induction of apoptosis in gastric cancer cells, which was due to a significant inhibitory action of PPIs on MAPK activation. 27 As Strowski and colleagues 13 reported that H pylori stimulated host VEGF gene expression via the MAPK pathway, we hypothesised that PPIs could exert antiangiogenesis actions through MAPK inhibition in H pylori induced angiogenesis.…”

mentioning

confidence: 99%

Novel action of gastric proton pump inhibitor on suppression of Helicobacter pylori induced angiogenesis

Yeo

2006

Gut

View full text Add to dashboard Cite

Background: Although activation of mitogen activated protein kinases (MAPKs) by Helicobacter pylori infection is associated with induction of host angiogenesis, which may contribute to H pylori associated gastric carcinogenesis, the strategy for its prevention has not been identified. As we previously reported a strong inhibitory action of gastric proton pump inhibitors (PPIs) on MAPK extracellular signal regulated kinase (ERK)1/2 phosphorylation, we investigated whether PPIs could suppress the H pylori induced angiogenesis via inhibition of MAPK ERK1/2. Methods: To address the relationship between H pylori infection and angiogenesis, comparative analysis of density of CD34+ blood vessel was performed in tissues obtained from 20 H pylori positive gastritis and 18 H pylori negative gastritis patients. Expression of hypoxia inducible factor 1 (HIF-1a) and vascular endothelial growth factor (VEGF) was tested by reverse transcription-polymerase chain reaction and secretion of interleukin 8, and VEGF was measured by ELISA. To evaluate the direct effect of H pylori infection on the tubular formation of human umbilical vein endothelial cells (HUVEC), an in vitro angiogenesis assay was employed. Activation of MAPK and nuclear factor kB (NFkB) was detected by immunoblotting.Results: H pylori positive gastritis patients showed a higher density of CD34 + blood vessels (mean 40.9 (SEM 4.4)) than H pylori negative gastritis patients (7.2¡0.8), which was well correlated with expression of HIF-1a. Conditioned media from H pylori infected gastric epithelial cells directly induced tubular formation of HUVEC and the increase of in vitro angiogenesis was suppressed by PPI treatment. Infection of H pylori significantly upregulated expression of HIF-1a and VEGF in gastric epithelial cells and expression of proangiogenic factors was mediated by MAPK activation and partially responsible for NFkB activation. PPIs effectively inhibited the phosphorylation of MAPK ERK1/2 that is a principal signal for H pylori induced angiogenesis. Conclusions: The fact that PPIs could downregulate H pylori induced angiogenesis indicates that antiangiogenic treatment using a PPI could be a promising protective therapeutic approach for H pylori associated carcinogenesis.

show abstract

A proton pump inhibitor, E3810, has an antibacterial activity through binding to Helicobacter pylori

Cited by 24 publications

References 0 publications

Potent Gastric Acid Inhibition in Helicobacter pylori Eradication

Potent Gastric Acid Inhibition in Helicobacter pylori Eradication

Rabeprazole‐based eradication therapy for Helicobacter pylori: a large‐scale study in Japan

Novel action of gastric proton pump inhibitor on suppression of Helicobacter pylori induced angiogenesis

Contact Info

Product

Resources

About