• Proceedings of the Korean Society of Postharvest Science and Technology of Agricultural Products Conference
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• 2007.11a
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• pp.227.1-227.1
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• 2007

• Korean Journal of Microbiology
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• v.41 no.2
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• pp.152-156
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• 2005

In the present study, lactic acid bacterium that has antibacterial activity against Helicobacter pylori was isolated from feces of newborn baby. The selection was based on the ability to inhibit the growth of H. pylori and to withstand harsh environmental conditions such as acidic pH and high bile concentration. By biochemical test and 16S rDNA sequencing, selected strain was turned out to be an Pediococcus acidilactici, therefore designated to P. acidilactici GMB7330. In order to investigate the inhibitory effects of P. acidilactici GMB7330 on the growth of H. pylori, we have tested in vitro studies such as cell viability and urease test. These results showed that antibacterial activity of P. acidilactici GMB7330 significantly decreased the viable cell count and urease activity of H. pylori. Antibacterial activity of P. acidilactici GMB7330 against H. pylori remained after pH adjustment to neutral, and the concentration of lactate produced from P. acidilactici GMB7330 was not enough to inhibit H. pylori. On the basis of the analysis by transmission electron microscope, it demonstrated that addition of P. acidilactici GMB7330 destroyed the cell structure of H. pylori. These results strongly suggested that P. acidilactici GMB7330 produce antibacterial substances to be able to inhibit the growth of H. pylori other than lactic acid.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.4 no.1
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• pp.10-17
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• 2001

Purpose: We measured anti-H. pylori IgG in Korean elementary school children living in Shinchon area of Seoul, Korea to evaluate the influence of environmental living standards on H. pylori infection. Methods: IgG antibodies to H. pylori were measured in plasma using a commercial ELISA kit (GAP IgG Helicobacter pylori, Bio-Rad Laboratories Inc., Hercules, CA, USA). Information on environmental status such as place of birth, parental income, type of housing, number of persons in the household, parents' occupation, family history of peptic ulcer disease and gastric cancer was obtained. Statistical analysis was done by Chi-square and logistic regression test using SPSS $7.0^{TM}$ for Windows. Results: Study subjects consisted of 571 children, and the age distribution ranged from 6.0 to 13.6 years with a mean of $9.6{\pm}1.8$ years. Male-to-female ratio was 1.1:1. The seropositive rates of H. pylori infection ranged from 10.4% in children aged 6 years to 30.9% in 12 year-old group, overall 16.8%. The prevalence of H. pylori infection progressively increased with age, but there was no significant difference in seropositive rates among children in different age groups (p=0.06). Seropositive rates of anti-H. pylori IgG on the basis of gender, place of birth, parental income, type of housing, parents' occupation, family history of peptic ulcer disease and gastric cancer showed no statistically significant difference. Interestingly, however, seropositive rate of anti-H. pylori IgG showed statistical significance in relation to number of persons in the household (p=0.003; Odds ratio 1.50 by logistic regression test). Conclusion: These results suggest that number of persons in the household is the most important factor among environmental living standards, and that risk of H. pylori infection increases by increment of 1.5 times as the number of persons in the household increases by one.

• Korean Journal of Pharmacognosy
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• v.33 no.4 s.131
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• pp.389-394
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• 2002

Present study was carried out for development of a new supplementary product with gastroprotective effect. Natural Products mentioned that have GI protective property in Dongeuibogam and reports were evaluated anti-bacterial activity against Helicobacter pylori, then five heres were selected. The material used for the test were water extract of Alpinia oxyphlla (AO), Astragalus membranaceus (AM), Cinnamomum loureirii(CL), Citrus aurantium(CA), Amomum villosum(AV). They were tested individually on HCI ethanol-induced gastric lesion in rats, AV CL, AO showed the most significant effectiveness, respectively. Then two mixture different in their content ratio (P020701-1,-2) and complex with P020701-1 (CP) were made, and tested on HCI·ethanol, indomethacin-induced gastric lesion, aspirin-ligature, Shay ulcer and gastric secretion. P020701-1, -2 and CP showed significant effect on HCI ethanol, indomethacin-induced gastric lesion, and Shay ulcer. It can be regarded that the antigasuitic and anti-ulcerative effects of P020701- 1, -2 and CP are originated from reduction of total acid output identified by gastric secretion test.

• Korean Journal of Clinical Pharmacy
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• v.7 no.1
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• pp.40-44
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• 1997

Helicobacter pylori(HP) has been implicated as the cause of acute and chronic gastritis, peptic ulcer, and gastric carcinoma. To date the most successful treatment in eradicating HP is known to be the combination of two or more antibiotics with an anti-ulcer drug. In this study, in vitro antimicrobial activity against two was assessed, when proton pump inhibitors (PPIs), omeprazole and lansoprazole, were added to antibiotics at different concentrations. The assays in the absence of PPIs gave minimum inhibitory concentration(MIC) value of 0.63 mg/l for amoxicillin, 4 mg/l for tetracycline, 0.08 mg/l for clarithromycin and 0.16 mg/l for azithromycin. At the concentrations of 125 mg/l, 25 mg/1 and 0.5 mg/l of omeprazole, and the concentrations of 31.25 mg/l, 6.25 mg/l and 1 mg/l of lansoprazole, the MICs of clarithromycin and azithromycin were reduced by $50\%$. Also, lansoprazole at the highest concentration 31.25 mg/l reduced the MIC of amoxicillin by $50\%$, and omeprazole at the highest concentration of 125 mg/l reduced the MIC of tetracycline by $50\%$. In conclusion, the in vitro combination of PPIs and antibiotics led to improvement in the MIC of antibiotics against HP associated gastric disease.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.17
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• pp.7911-7916
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• 2015

Serum anti-Helicobacter pylori antibodies and pepsinogens (PGs) have been used as gastric cancer screening and gastric mucosal status markers. Nepal is a low risk country for gastric cancer. However, the mountainous populace in the northern region culturally linked to Tibet as well as Bhutan, a neighboring country, have a high risk of GC. We collected gastric biopsy specimens and sera from 146 dyspeptic patients living in Kathmandu, Nepal. We also examined the sera of 80 volunteers living in the mountainous regions of the Himalayas. The optimal cut-off was calculated for serum biomarkers against the histology. Kathmandu patients (43.8%) were serologically positive for H. pylori infection, which was significantly lower than that for the mountainous (61.3%, P = 0.01). The same results also found in the prevalence of PG-positivity, PG I levels and PG I/II ratios (P = 0.001, P<0.0001 and P = 0.03, respectively). Moreover, the PG I/II ratios were significantly, and inversely correlated with the OLGA score (r = -0.33, P<0.009). The low incidence of gastric cancer in Nepal can be attributed to low gastric mucosal atrophy. However, the mountainous subjects have high-risk gastric mucosal status, which could be considered a high-risk population in Nepal.

• Journal of Life Science
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• v.26 no.10
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• pp.1214-1217
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• 2016

Rebamipide is a mucosal-protective antiulcer drug, but its mechanism of action in gastric cancer remains elusive. CagA, a major virulence factor of Helicobacter pylori (H. pylori), is associated with the risk of gastric cancer. CagA protein is injected into gastric epithelial cells and deregulates a variety of cellular signaling molecules. CagA from H. pylori induces phospholipase D1 (PLD1) expression through NFκB activation in gastric epithelial cells, followed by invasion and proliferation of gastric epithelial cancer cells. Infection with cagA-positive H. pylori and expression of CagA enhances the binding of NFκB to the PLD1 promoter. Rebamipide abolishes H. pylori cagA-induced PLD1 expression via inhibition of binding of NFκB to the PLD1 promoter and also inhibits PLD activity. Moreover, rebamipide abolishes H. pylori CagA-induced β-catenin and the expression of a target cancer stem cell (CSC) marker gene via upregulation of miRNA-320a and -4496, followed by attenuation of self-renewal capacity of H. pylori CagA-infected gastric CSCs. In addition, rebamipide increases the chemosensitivity of CagA-expressed gastric CSCs and suppresses gastric carcinogenesis. Thus, it is speculated that rebamipide might show a potent efficacy as chemotherapeutic drug against gastric cancer cells. In this review, we summarizes recent results regarding the novel insights for the efficacy of rebamipide in gastric cancer cells.

• Biomolecules & Therapeutics
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• v.29 no.4
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• pp.410-418
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• 2021

Helicobacter pylori causes chronic gastritis through cag pathogenicity island (cagPAI), vacuolating cytotoxin A (VacA), lipopolysaccharides (LPS), and flagellin as pathogen-related molecular patterns (PAMPs), which, in combination with the pattern recognition receptors (PRRs) of host cells promotes the expression and secretion of inflammation-causing cytokines and activates innate immune responses such as inflammasomes. To identify useful compounds against H. pylori-associated gastric disorders, the effect of chalcone derivatives to activate the nucleotide-binding oligomerization domain (NOD)-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome was examined in an H. pylori-infected human monocytic THP-1 cell line in this study. Among the five synthetic structurally-related chalcone derivatives examined, 2'-hydroxy-4',6'-dimethoxychalcone (8) and 2'-hydroxy-3,4,5-trimethoxychalcone (12) strongly blocked the NLRP3 inflammasome in H. pylori-infected THP-1 cells. At 10 μM, these compounds inhibited the production of active IL-1β, IL-18, and caspase-1, and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) oligomerization, but did not affect the expression levels of NLRP3, ASC, and pro-caspase-1. The interruption of NLRP3 inflammasome activation by these compounds was found to be mediated via the inhibition of the interleukin-1 receptor-associated kinase 4 (IRAK4)/IκBα/NF-κB signaling pathway. These compounds also inhibited caspase-4 production associated with non-canonical NLRP3 inflammasome activation. These results show for the first time that certain chalcones could interrupt the activation of the NLRP3 inflammasome in H. pylori-infected THP-1 cells. Therefore, these chalcones may be helpful in alleviating H. pylori-related inflammatory disorders including chronic gastritis.

• Biomolecules & Therapeutics
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• v.16 no.3
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• pp.270-276
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• 2008

In this study we investigated the effects of Magnolia Bark (MB) extract and its constituents, such as honokiol and magnolol, on gastritis in rats and the growth of human gastric cancer cells. The MB extract, honokiol, and magnolol showed the acid-neutralizing capacities, the antioxidant activities, and the inhibitory effect on the growth of Helicobacter pylori (H. pylori.) at the dose of $50\;{\mu}g/ml$ and over, which is equivalent to that of ampicillin ($100\;{\mu}g/ml$). Honokiol and magnolol had no significant cytotoxicity to human gastric caner cells (AGS and SNU638). However, the MB extract had cytotoxic activity against AGS gastric cancer cell. The MB extract, honokiol, and magnolol significantly inhibited HCI-ethanol-induced gastric lesions without clear change of mucus content. In pylorus ligated rats, honokiol significantly decreased the volume of gastric secretion and gastric acid output, and increased the pH. Magnolol increased the mucus content to almost the same as the control group at oral doses of 50 mg/kg. Therefore, we could guess that antigastritic action of honokiol and magnolol may be associated with the antioxidant activities, acid-neutralizing capacities, inhibition of secretion in gastric acid, and anti-H. pylori action. From these results, we could suggest that MB extract and its constituents, such as honokiol and magnolol, may be useful for the treatment and/or protection of gastritis.

• Journal of Microbiology and Biotechnology
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• v.16 no.2
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• pp.318-324
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• 2006

In order to develop an oral vaccine to prevent H. pylori infection, we have expressed the hpaA gene of H. pylori K51 isolated from Korean patients, encoding 29-kDa HpaA that is known to be localized on the cell surface and flagella sheath, in a live delivery vector system, Lactococcus lactis. The hpaA gene, amplified by PCR using the genomic DNA of H. pylori K51, was cloned in the pGEX-2T vector, and the DNA sequence analysis revealed that the hpaA gene of H. pylori K51 had 99.7% and 94.8% identity with individual hpaA genes of the H. pylori 26695 strain (U.K) and the J99 strain (U.S.A). A polyclonal anti-HpaA antibody was raised in rats using GST-HpaA fusion protein as the antigen. The hpaA gene was inserted in an E. coli-L. lactis-shuttle vector (pMG36e) to express in L. lactis. Western blot analysis showed that the expression level of HpaA in the L. lactis transformant remained constant from the exponential phase to the stationary phase, without extracelluar secretion. These results indicate that the HpaA of H. pylori K51 was successfully expressed in L. lactis, and suggest that the recombinant L. lactis expressing HpaA may be applicable as an oral vaccine to induce a protective immune response against H. pylori.