• Journal of Microbiology and Biotechnology
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• v.25 no.10
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• pp.1629-1633
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• 2015

Peptide assimilation in Helicobacter pylori necessitates a coordinated working of the peptide transport systems (PepTs) and aminopeptidase (PepA). We found that H. pylori hydrolyzes two detector peptides, _L-phenylalanyl- _L-3-thiaphenylalanine (PSP) and _L-phenylalanyl- _L-2-sulfanilylglycine (PSG), primarily before intake and excludes their antibacterial effects, whereas Escherichia coli readily transports them with resultant growth inhibition. PSP assimilation by H. pylori was inhibited by aminopeptidase inhibitor bestatin, but not by dialanine or cyanide-m-chlorophenylhydrazone, contrary to that of E. coli. RT- and qRT-PCR analyses showed that H. pylori may express first the PepTs (e.g., DppA and DppB) and then PepA. In addition, western blot analysis of PepA suggested that the bacterium secretes PepA in response to specific inducers.

• Journal of Microbiology and Biotechnology
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• v.13 no.5
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• pp.666-672
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• 2003

Vacuolar degeneration of the gastric epithelial cells is a characteristic feature of the derangement of mucosa where Helicobacter pylori colonizes, and H. pylori vacuolating cytotoxin (VacA) has been suggested to playa key role in it. To elucidate the VacA-involved degenerative mechanism, VacA was purified, and its impact on degeneration of HeLa cells was determined. In the presence of ammonium chloride, cell vacuolation by VacA was dose-and time-dependent, however, no detectable degeneration of the cells was observed with the VacA concentration tested. A further increase of vacuolation was shown in cells pre-treated with diethyl pyrocarbonate (DEPC) , and this resulted in a change of the cell morphology to become spherical. Similar phenomena were also observed when HeLa cells were co-cultivated with intact H. pylori cells. It was remarkable to note that the degree of growth inhibition was proportional to the increase in vacuole formation, suggesting that the vacuolation rate would be critical for cell degeneration. Surprisingly, although VacA was itself inhibited by DEPC, its uptake was markedly increased by this agent, similar to that found in cells with Nabutyrate. These data indicate that the cell's tolerance of VacA transport may be critical for vacuolar degeneration and may be changeable during H. pylori inhabitation.

• Korean Chemical Engineering Research
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• v.51 no.5
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• pp.591-596
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• 2013

Urease activity of Helicobacter pylori was most strongly inhibited by extract of Mume Fructus among ethanol (70%, v/v) extract of 6 herbal materials selected from our previous work, database on traditional herbal materials, and literature data on Korean plant resources. Active compounds in the extract of Mume Fructus were separated by batch extraction, and further purified by chromatography in a silica gel column and an octadecyl silica gel column using solvents of different polarity. By NMR analysis of the last chromatographic fraction we identified ursolic acid as the active compound of urease inhibition. The result suggests that this component in Mume Fructus can possibly be used for the eradication of H. pylori.

• Journal of Applied Biological Chemistry
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• v.55 no.3
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• pp.169-172
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• 2012

The aim of this research was to investigate the antibacterial activity of Clerodendron trichotomum. Antibacterial activities of the n-hexane, methylene chloride (MC), ethyl acetate, and n-butanol fractions from C. trichotomum were tested against Staphylococcus aureus, Escherichia coli, and Helicobacter pylori. The n-hexane and MC fractions showed antibacterial activity against H. pylori at a concentration of 1.7 mg/mL and showed inhibition zones of 10 and 11 mm in disc assay, respectively. Further testing of 22-dehydroclerosterol and ${\beta}$-amyrin (each 3.4 mg/mL) from the MC fraction of C. trichotomum revealed moderate antibacterial effects against E. coli, S. aureus, and H. pylori. In particular, ${\beta}$-amyrin showed clear zones of 12 and 13 mm against E. coli and H. pylori, respectively, suggesting its potential as an antibacterial agent. The active compounds from C. trichotomum might provide a promising therapeutic agent against infections by E. coli, S. aureus, and H. pylori.

• Asian-Australasian Journal of Animal Sciences
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• v.15 no.7
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• pp.1057-1065
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• 2002

The antagonistic activities of 30 strains of lactobacilli against Helicobacter pylori were determined and Lactobacillus helveticus CU631 has been selected as the strain which possesses the strongest inhibitory effect in the disc diffusion assay showing inhibition zone diameter of $10{\pm}1.5mm$, whereas those of L. plantarum and L. fermentum have been shown to be $4.0{\pm}0.6mm$. H. pylori G88016 revealed the highest vacuolating toxin producing activity among the 8 strains, the inhibitory activity of L. helveticus CU631 in vacuolating toxin producing activity of H. pylori manifested in the co-culture of two strains and in the 5:5 mixture of supernatant of the two strains. Both L. helveticus CU631 and cell free culture supernatant had a strong inhibitory activities in urease and cytotoxin producing activities of H. pylori NCTC11637 and CJH12. An accelerated proteolytic activity of water soluble peptides by L. helveticus CU631 during the refrigeration storage has been manifested in the cream cheese. DNA seqences of 16S-23S ribosomal RNA spacer region showed typical pattern among the various strains of L. helveticus, which could be used in the identification of L. helveticus CU 631.

• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.5005-5006
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• 2015

Gastric cancer as one of the most common cancers worldwide has various genetic and environmental risk factors including Helicobacter pylori (H.pylori) infection. Recently, loss of a tumor suppressor gene named promyelocytic leukemia (PML) has been identified in gastric cancer. However, no mutation has been found in this gene in gastric cancer samples. Cag A H.pylori protein has been shown to exert post transcriptional regulation of some tumor suppressor genes. In order to assess such a mechanism for PML degradation, we performed in silico analyses to establish any interaction between PML and Cag A proteins. In silico interaction and docking studies showed that these two proteins may have stable interactions. In addition, we showed that imatinib kinase inhibitor can restore PML function by inhibition of casein kinase 2.

• Biomolecules & Therapeutics
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• v.23 no.1
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• pp.53-59
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• 2015

In this study, we investigated the inhibitory activities on gastritis and gastric ulcer using liriodendrin which is a constituent isolated from Kalopanax pictus. To elucidate its abilities to prevent gastric injury, we measured the quantity of prostaglandin $E_2$ ($PGE_2$) as the protective factor, and we assessed inhibition of activities related to excessive gastric acid be notorious for aggressive factor and inhibition of Helicobacter pylori (H. pylori) colonization known as a cause of chronic gastritis, gastric ulcer, and gastric cancer. Liriodendrin exhibited higher $PGE_2$ level than rebamipide used as a positive control group at the dose of $500{\mu}M$. It was also exhibited acid-neutralizing capacity (10.3%) and $H^+/K^+$-ATPase inhibition of 42.6% ($500{\mu}M$). In pylorus-ligated rats, liriodendrin showed lower volume of gastric juice ($4.38{\pm}2.14ml$), slightly higher pH ($1.53{\pm}0.41$), and smaller total acid output ($0.47{\pm}0.3mEq/4hrs$) than the control group. Furthermore liriodendrin inhibited colonization of H. pylori effectively. In vivo test, liriodendrin significantly inhibited both of HCl/EtOH-induced gastritis (46.9 %) and indomethacin-induced gastric ulcer (46.1%). From these results, we suggest that liriodendrin could be utilized for the treatment and/or protection of gastritis and gastric ulcer.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8883-8886
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• 2014

Background: Tetracycline is an antibiotic widely used for the treatment of Helicobacter pylori infection, but its effectiveness is decreasing due to increasing bacterial resistance. The aim of this study was to investigate the occurrence of 16S rRNA mutations associated with resistance or reduced susceptibility to tetracycline ofHelicobacter pylori by real-time PCR (RT-PCR) assays from culture. Materials and Methods: Tetracycline susceptibility and minimal inhibition concentration (MIC) was determined by the Epsilometer test (Etest) method. A LightCycler assay developed to detect these mutations was applied to DNA extracted from culture. The 16S rRNA of these isolates was sequenced and resistance-associated mutations were identified. From 104 isolates of H. pylori examined, 11 showed resistance to tetracycline. Results: LightCycler assay was applied to DNA extracted from 11 tetracycline-susceptible and 11 tetracycline resistance H. pylori isolates. In our study the sequencing of the H. pylori wild types in 16 s rRNA gene were AGA 926-928 with MIC (0.016 to $0.5{\mu}g/ml$), while the sequencing and MIC for resistant were GGA and AGC, (0.75 to $1.5{\mu}g/ml$), respectively. Also we found a novel mutation in 2 strains with $84^{\circ}C$ as their melting temperatures and exhibition of an A939C mutation. Conclusions: We conclude that real-time PCR is an excellent method for determination of H. pylori tetracycline resistance related mutations that could be used directly on biopsy specimens.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.99-110
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• 1999

Effects of Chiyangtang(CYT) on H. pylori-induced increase of interleukin 8 and interleukin 1 gene expression was studied in Kato Ⅲ cell line, a human stomach epithelial cell line. Treatment of H. pylori to the cell culture signifant!y increased IL-8 and IL-1 mRNA synthesis. When CYT was added along with H. pylori, the increase of IL-8 and IL-1 mRNA synthesis was blocked. Activation of transcription factor $NF-{\kappa}B$ and AP-1 which were known to important in IL-8 and IL-1 gene expression was also studied using chloramphenicol acetyltransferase(CAT) assay. Treatment of H. pylori increased activation of $NF-{\kappa}B$ and AP-l and CYT effectively protected the activation. Electrophoretic mobility shift assay suggested that CYT effectively inhibited DNA binding of $NF-{\kappa}B$ and AP-l to their cognate site. These results suggested that CYT could prevent stomach diseases through the down regulation of IL -8 and IL-l gene expression which might be mediated by the inhibition of $NF-{\kappa}B$ and AP-1 activities and their binding to DNA.