• 제목/요약/키워드: H. pylori inhibition

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헬리코박터 파이로리균에 대한 약용식물의 항균 효과 (Antibacterial effect of medicinal plants against Helicobacter pylori)

  • 이재혁;김정숙;박정숙
    • 디지털융복합연구
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    • 제17권2호
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    • pp.447-451
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    • 2019
  • 본 연구는 건강식품으로 많이 사용되는 32종의 약용식물에 대한 헬리코박터 파이로리 항균효과를 살펴보기 위해서 디자인되었다. 연구에 사용된 약용식물은 모든 사람들이 매일 먹을 수 있는 것으로 H.pylori 활성에 대한 디스크 확산법을 이용하여 32종의 약용식물 추출물을 사용하였고 Amoxicillin sodium (150mg/ml,일동제약)과 메트로니다졸 (Metronidazol, 50mg/ml)을 대조군으로 사용하였다. 투명한 영역의 면적을 측정하고 그 면적이 더 큰 크기가 H. pylori에 많은 효과가 있다고 평가했다. 이 연구의 결과, 고련피 억제 값은 $372.90mm^2$로 가장 높았고, 둘째, 오배자 $358.30mm^2$, 그리고 청호 $348.32mm^2$이었다. 양성 대조군인 Metronidazole (50mg / ml CJ) 값은 $503,29mm^2$이었다. 향후 H. pylori 억제를 위해 다양한 약용식물의 항균소재개발이 가치가 있을 것으로 사료된다.

Enzyme-Linked, Biotin-Streptavidin Bacterial-Adhesion Assay for Helicobacter pylori Lectin-Like Interactions with Cultured Cells

  • Murillo, Guzman;Antonia, Maria;Ascencio, Felipe
    • Journal of Microbiology and Biotechnology
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    • 제11권1호
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    • pp.35-39
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    • 2001
  • A simple method for studying the lectin-like interactions between Helicobacter pylori and cultured human epithelial cell lines was developed using an enzyme-linked, biotin-streptavidin bacterial-adhesion assay. The present study suggests that this method is suitable for evaluating the participation of lectin interactions in the adhesion of H. pylori to cultured HeLa S3 and Kato III cells, both fixed and glycosidase-treated cells, as well as assessing glycoconjugated binding inhibition studies. The time-course and dose-dependent kinetics of the biotin-labeled H. pylori adhesion th the formaldehyde-fixed Hela S3 and Kato III cell lines exhibited saturation. In addition, the binding of the biotin-labeled H. pylori to the formaldehyde-fixed cultured cells was partially blocked by pre-incubation with glycoconjugates and polyclonal antibodies against a heparan sulfate binding protein from H. pylori.

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곰팡이에서 분리한 Helicobacter pylori 항균물질의 분리 및 구조규명 (Isolation and Structural Determination of Anti-Helicobacter pylori Compound from Fungus 60686.)

  • 남궁준;연승우;백남수;김태한;김영호;김창진;김기원
    • 한국미생물·생명공학회지
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    • 제26권2호
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    • pp.137-142
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    • 1998
  • 본 실험에서는 만성위염, 위궤양, 십이지장궤양, 위암발생의 원인균으로 알려진 H. pylori를 저해하는 특이항균물질을 생성하는 균주를 토양에서 분리한 방선균액과 곰팡이 추출액을 대상으로 탐색하여 곰팡이 균주번호 60686을 선별하였다. Jar fermentor로 배양하여 얻은 균체를 acetone 및 EtOAc로 추출하였고, 얻어진 추출액을 silica column chromatography와 LH-20 gel chromatography를 수행하여 활성분획을 농축하였고 HPLC를 사용하여 항균 활성을 나타내는 단일물질 IDA를 분리 정제하였다. 항균 활성물질 IDA의 구조를 MS, NMR 분석등을 통해 추정한 결과 곰팡이의 2차 대사산물인 cytochalasan의 전형적 구조를 갖는 분자식 $C_{32}H_{36}N_2O_5$의 chaetoglobosin A라는 물질로 판명되었다. 항균물질 IDA의 항균력을 paper disk법으로 실험한 결과 그람양성 균주중에서는 S. aureus SG 511, 285와 503 3주에서만 항균력을 보였고, 그람음성 균주중에서는 H. pylori 4주에서만 항균력을 보였으나 동일농도 처리시 H. pylori에 대한 항균력이 S. aureus에 비해 우수한 항균효과를 가진다고 판단되었다.

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김치와 타락에서 분리한 젖산균의 Helicobacterpylori에 대한 항균 효과 (Antimicrobial Effect of Lactic Acid Bacteria Isolated from Kimchi and Tarak on Helicobacter pylori)

  • 이영덕;유혜림;황지연;한복경;최혁준;박종현
    • 한국식품영양학회지
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    • 제23권4호
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    • pp.664-669
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    • 2010
  • 한국인의 주된 위 건강의 저해인자인 Helicobacter pylori를 저해하는 젖산균을 타락과 김치에서 분리하여 특성을 분석하고자 하였다. 전통발효 젖산균음료인 타락 5개와 김치 30종을 안동 지역과 수도권의 시장에서 구입하고, 젖산균을 전통적인 분리방법에 따라 15주를 분리하였다. 이들 젖산균에 대하여 H. pylori 생육 저해 활성이 높은 두 개의 젖산균을 선택하여 동정하였다. 이들 젖산균은 전형적인 생화학적인 특성과 16S DNA의 분석을 통하여 타락에서 분리된 균은 Streptococcus thermophilus LAB kw15로 김치에서 분리된 균은 Leuconostoc mesenteroides LAB kw5로 동정하였다. 이들 분리 균주 배양액을 중성으로 조정한 후 첨가하여 배양할 때 H. pylori의 생육을 현저히 저해하였으며, H. pylori와의 혼합 배양에서도 H. pylori의 생육을 저해하는 것으로 나타났다. 그러므로 이 분리 젖산균의 대사산물이 H. pylori의 생육을 저해하고 있는 것으로 나타나, 기능성 젖산균으로의 활용이 가능할 것으로 판단된다.

Inhibitory Activities of Palmatine from Coptis chinensis Against Helicobactor pylori and Gastric Damage

  • Jung, Joohee;Choi, Jae Sue;Jeong, Choon-Sik
    • Toxicological Research
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    • 제30권1호
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    • pp.45-48
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    • 2014
  • Helicobacter pylori (H. pylori) is the most important factor of gastric disease in clinical practice. Moreover, smoking, stress and a poor diet may be additive factors for gastric damage. With these factors, increasing infection of H. pylori triggers gastritis, gastric ulcers and gastric cancer. To develop a new protective agent, we are concerned with plant-derived extract. The extract of Coptis chinensis (C. chinensis) and its constituents were investigated to assess their protective activities against gastric damage. The C. chinensis extract showed a scavenging effect against 2, 2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide radicals, inhibition of H. pylori colonization and antiulcerogenic activities in rat. In particular, palmatine derived from C. chinensis was found to be the novel protective agent. It is better than the C. chinensis extract, berberine, a well-known constituent of C. chinensis. We suggest that palmatine from the root cortex of C. chinensis may be a good candidate for the development of new pharmaceuticals to prevent gastric disease.

Inhibitory Effect of Capsaicin on Interleukin-8 Production by Helicobacter pylori-Infected MKN-45 Cells

  • Lee, Kwang-Hyoung;Lee, Yong-Chan;Kim, Tae-Il;Noh, Sung-Hoon;Kim, Ji-Yeon;Paik, Hyun-Dong;Kim, Chang-Han
    • Journal of Microbiology and Biotechnology
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    • 제16권7호
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    • pp.1078-1083
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    • 2006
  • Capsaicin is the active ingredient in chili pepper and has an inhibitory effect on Helicobacter pylori growth and $NF-{\kappa}B$ activation. The present study examined the effect of capsaicin on interleukin (IL)-8 production by H. pylori ATCC 43504-infected MKN-45 cells, a gastric epithelial cell line. The viability of the MKN-45 cells treated with capsaicin at 0, 50, 100, 250, and $500\;{\mu}M$ was 99, 98, 99, 99, and 85%, respectively. A capsaicin concentration as low as $50\;{\mu}M$ significantly inhibited the IL-8 production induced by H. pylori ATCC 43504 infection (43.2% of control) during 24 h of incubation. However, low concentrations of capsaicin $(50\;and\;100{\mu}M)$ did not significantly inhibit the IL-8 production by $TNF-{\alpha}-$ or PMA-treated MKN-45 cells. Therefore, the overall inhibitory effect of capsaicin on H. pylori ATCC 43504 was the sum of H. pylori ATCC 43504 growth inhibition, host cell survival, and $NF-{\kappa}B$ signal cascade inhibition.

MicroRNA-146a Enhances Helicobacter pylori Induced Cell Apoptosis in Human Gastric Cancer Epithelial Cells

  • Wu, Kai;Yang, Liu;Li, Cong;Zhu, Chao-Hui;Wang, Xin;Yao, Yi;Jia, Yu-Jie
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권14호
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    • pp.5583-5586
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    • 2014
  • Helicobacter pylori (H. pylori) infection induces apoptosis in gastric epithelial cells, and this occurrence may link to gastric carcinogenesis. However, the regulatory mechanism of H. pylori-induced apoptosis is not clear. MicroRNA-146a has been implicated as a key regulator of the immune system. This report describes our discovery of molecular mechanisms of microRNA-146a regulation of apoptosis in human gastric cancer cells. We found that overexpression of microRNA-146a by transfecting microRNA-146a mimics could significantly enhance apoptosis, and this upregulation was triggered by COX-2 inhibition. Furthermore, we found that microRNA-146a density was positively correlated with apoptosis rates in H. pylori-positive gastric cancer tissues and intratumoral microRNA-146a density was negatively correlated with lymph node metastasis among H. pylori-positive gastric cancer patients. Understanding the important roles of microRNA-146a in regulating cell apoptosis in H. pylori infected human gastric cancer cells will contribute to the development of microRNA targeted therapy in the future.

Emodin Attenuates Inflammasome Activation Induced by Helicobacter pylori Infection through Inhibition of VacA Translocation

  • Thach Phan Van;Anh Duy Do
    • 한국미생물·생명공학회지
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    • 제51권4호
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    • pp.507-516
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    • 2023
  • Eradication of Helicobacter pylori infection is an essential strategy to decrease the risk of developing gastric cancer. However, the standard triple therapy has negative aspects associated with side effects and the emergence of antibiotic resistance. Therefore, alternative therapies are required to enhance the management of H. pylori infection effectively. In this study we examined the effect of emodin on the amelioration of inflammatory response due to H. pylori infection. Our results indicated that emodin treatment effectively decreased the expression of virulence genes, including sabA, vacA, cagL, cagA, sabA, and suppressed the adhesion ability of H. pylori to AGS cells. Emodin has been shown inhibitory effects on the inflammasome pathway through reductions in VacA translocation, lowering ROS stress, cleaved Caspase-1, NLRP3, and cleaved Gasdermin D levels, thereby lowered pyroptosis in infected cells. In summary, our study demonstrated that emodin has the ability to attenuate inflammation caused by H. pylori by modulating virulence gene expression and decreasing VacA translocation. Further study is required to evaluate the therapeutic efficacy of emodin in treating H. pylori infection and better understand the underlying mechanisms.

Inhibitory Effects of 4-Guanidinobutyric Acid against Gastric Lesions

  • Hwang, In-Young;Jeong, Choon-Sik
    • Biomolecules & Therapeutics
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    • 제20권2호
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    • pp.239-244
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    • 2012
  • This study examined the inhibitory effects of 4-guanidinobutyric acid (4GBA), an alkaloid, against gastric lesions by assessing the inhibition of Helicobacter pylori (H. pylori) and gastric cancer cells. Acute and chronic gastritis were also observed using HCl/ethanol (EtOH) and indomethacin-induced gastric lesion models, respectively. 4GBA inhibited the growth of H. pylori in a dose dependent manner, and showed acid-neutralizing capacity. In the pylorus ligated rats, 4GBA decreased the volume of gastric secretion and gastric acid output slightly, and increased the pH. 4GBA at a dose of 100 mg/kg reduced the size of HCl/EtOH-induced gastric lesions (70.8%) and indomethacin-induced gastric lesions (38.8%). The antigastritic action of 4GBA might be associated with the acid-neutralizing capacity, anti-H. pylori action, and decreased volume of gastric secretion. These results suggest that 4GBA might be useful in the treatment and/or protection of gastritis.

위염 및 Helicobacter pylori에 미치는 Amomi Semen Butanol 추출물의 영향 (Effects of Amomi Semen Butanol Fraction on Gastritis and Helicobacter pylori)

  • 강민희;정춘식
    • 생약학회지
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    • 제35권4호통권139호
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    • pp.350-356
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    • 2004
  • In a preliminary screening of plant extracts for the antigastritic and anti- Helicobacter pylori (H. pylori) actions in rats, the ethanol extract of Amomi Semen (AS) showed positive activity in HCl Ethanol-induced gastric lesions and H. pylori. Among the systematic fractions of hexane, chloroform, butanol and water, the most potent butanol fraction significantly reduced HCl, Ethanol-induced gastric lesions at the oral dose of 350 mg/kg. Also butanol fraction has an inhibitory effect on the growth of H. pylori $(MIC=1.43\;{\mu}g/mL)$. In pylorus ligated rats, butanol fraction showed decrease in the volume of gastric secretion and acid output, of which effects were stronger in other fractions. We isolated 6 subfractions by column chromatography. The protective effects of 6 subfractions of Amomi Semen were also significant in the HCl, Ethanol induced gastric lesion model. These results might suggest that they had inhibitory action in gastric lesion through inhibition of gastric acid secretion. Butanol fraction of AS can be applied as treatment of H. pylori. Butano fractions and ethanol extract of AS was carried out or the development of a new gastroprotective supplementary product.