• 제목/요약/키워드: Colonic adhesion

검색결과 16건 처리시간 0.022초

Colonic mucin-binding assay를 이용한 장내 우수 점착능 유산균주의 선별 (Screening of Lactic Acid Bacteria with Potent Adhesive Property in Human Colon using Colonic Mucin-binding Assay)

  • 김성영;신광순;이호
    • 한국식품과학회지
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    • 제36권6호
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    • pp.959-967
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    • 2004
  • 인간의 대장내 점막에 대하여 우수한 점착특성을 갖는 probiotic 유산균주를 선별할 목적으로, colonic mucin-binding assay를 고안하고 최적의 분석 조건을 검토한 결과, microtiter plate의 well에 대한 colonic mucin의 부착은 pH 4.8, biotinylated SLP의 농도는 $5.0\;{\mu}g/mL$, 시판 HRP-conjugated streptoavidin은 24,000배 희석용액, TMB의 발색시간은 10분의 조건에서 측정시 최적의 결과를 나타냈다. 동 조건에서 본 assay system을 이용할 경우, 장내 점착능 측정 및 우수 유산균주의 선별에 있어 신속하고 재현성 있는 결과를 제공할 수 있으며, 인간의 대장에 대한 유산균의 점착특성을 정량적으로 분석할 수 있음을 보여주었다. 공시균주 32종 및 유아 분변 유래의 분리균주 18종을 포함한 총 50종의 유산균주에 대하여, colonic mucin-binding assay를 이용하여 대장 mucin에 대한 결합능을 비교한 결과, L. species FSB-1이 가장 높은 결합능을 보여주었다. 따라서 L. species FSB-1을 대상으로 형태학적 특성, 생리 및 생화학적 특성과 16S rDNA에 대한 부분 염기서열 분석을 포함한 동정실험을 수행한 결과, 장내 점착능 우수균주로 선별된 L. species FSB-1은 Lactobacillus brevis로 최종 동정되었다.

Functional Analysis of B7-H3 in Colonic Carcinoma Cells

  • Lu, Peng;Liu, Rong;Ma, Er-Min;Yang, Tie-Jian;Liu, Jia-Lin
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권8호
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    • pp.3899-3903
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    • 2012
  • B7-H3 is a newly discovered member of the B7/CD28 superfamily which functions as an important T-cell immune molecule. It has been reported recently that B7-H3 is highly expressed in many cancer cells, the data indicating that it may be a regulation factor contributing to tumor-resistance. In our study, we used bioinformatics to identify differentially expressed genes between colonic cancer cells and normal colonic cells, aiming to analyze mechanisms and identify sub-pathways closely related to progression, with the final aim of finding small molecule drugs which might interfere this progression. We found that ajmaline is one related factor which may enhance self-immunity in colon carcinoma therapy and B7-H3 plays important roles with regard to immunoreactions of colonic cancer cells. All the results indicate that H7-B3 is a favorable prognostic biomarker for colon carcinomas, providing novel information regarding likely targets for intervention.

Protective Effect of Taurine on TNBS-induced Inflammatory Bowel Disease in Rats

  • Son, Mi-Won;Ko, Jun-Il;Doh, Hyoun-Mie;Kim, Won-Bae;Park, Tae-Sun;Shim, Mi-Ja;Kim, Byong-Kak
    • Archives of Pharmacal Research
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    • 제21권5호
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    • pp.531-536
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    • 1998
  • We had previously reported that the protective effect of taurine against indomethacin-induced gastric mucosal injury was due to its antioxidant effects, which inhibited lipid peroxidation and neutrophil activation. In this study, we examined the effect of taurine on reducing the inflammatory parameters of trintrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease (IBD) in rats. In order to induce IBD, ethanolic TNBS was given to rats intracolonically. Then they received 500 mg/kg.day of taurine orally and were sacrificed one week after IBD induction. While ulceration and inflammation of distal colon with formation of granuloma in the vehicle-treated IBD rats two days after administration of TNBS were observed, treatment with taurine ameliorated colonic damage and decreased the incidence of diarrhea and adhesion. also, colon weight as an index of tissue edema, which was mardedly increased in the IBD rats, became significantly lower after administration of TNBS were observed, treatment with taurine ameliorated colonic damage and decreased the incidence of diarrhea and adhesion. Also colon weitht as an index of tissue edema, which was markedly increased in the IBD rats, became significantly lower after taruine treatment. Myeloperoxidase (MPO) activity in the vehicle-treated IBD rats was substantially increased, compared with that of normal control. the taurine-treated animals significantly reduced MPO activity (35% lower) when compared with that of the vehicle-treated animals. Taurine treatment decreased both basal and formyl-methionyl leucyl phenylalanine-stimulated reactive oxygen generation from colonic tissue in the IBD rats. These results suggest that the administration of taurine reduce the inflammatory parameters in this IBD rat model by increasing defending capacity against oxidative damage.

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새로운 플라보노이드 유도체인 DA-6034의 TNBS 유발성 염증성대장염 모델에서의 치료효과 (Effect of DA-6034, a New Flavonoid Derivative, on TNBS-Induced Colitis in the Rats)

  • 손미원;고준일;김희기;장동경;유무희;김원배;이강춘;송인성
    • 약학회지
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    • 제42권2호
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    • pp.205-213
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    • 1998
  • The efficacy of DA-6034, a new flavonoid derivative, was investigated in comparison with sulfasalazine in a trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. Under light anaesthesia with ether, rats were subjected to intracolonic administration of 30mg TNBS in 50% ethanol (0.5ml) and were then sacrificed at 7 or 21 days after colitis induction. The TNBS control group (the saline treated colitic rat) exhibited ulceration and inflammation of the distal colon with formation of granuloma and pathologic connections. Moreover, an increase in colonic myeloperoxidase (MPO) activity (investigated as an index of leukocyte adhesion and accumulation) and an elevated colonic leukotriene $B_4$ ($LTB_4$) level were observed. The colitic rats received DA6034 (0.3-30mg/kg) or sulfasalazine (50-100mg/kg), prednisolone (0.3-3mg/kg) after the induction of colitis until they were sacrificed. Oral treatment with DA-6034 resulted in significant reductions of macroscopic colonic damage, colonic inflammation. DA6034 had a more potent effect than sulfasalazine and prednisolone on macroscopic colonic damage, while it has similar effect with prednisolone on the reduction of colonic $LTB_4$ synthesis and MPO activity. This study show, therefore, that DA-6034 is effective m attenuating the colonic lesion in an TNBS-induced colitis model. Furthermore, the results suggest that the effect of DA-6034 is partially related to its action on $LTB_4$ synthesis and MPO inhibition.

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기관-흉강-위장-대장 누공 - 1예 보고 - (Broncho-Pleuro-Gastro-Colonic Fistula -A case report-)

  • 문성호;장인석;이정은;김종우;최준영;이상호
    • Journal of Chest Surgery
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    • 제43권2호
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    • pp.224-227
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    • 2010
  • 호흡기와 위장관 사이의 누공은 염증이나 외상에 의하여 발생된다. 저자들은 기관지-흉강-위장-대장 누공이 있는 51세 남자 환자를 경험하였다. 호흡시에 만성적인 악취를 호소하던 환자는 30년 전 횡격막파열의 기왕력을 가지고 있었다. 횡격막 염증이 좌하엽 괴사를 유발하여 기관지-흉강강 누공을 만들었고, 위장의 분문부과 대장의 비장굽이부분에 천공을 유발하였다. 저자들은 좌하엽 절제술과 횡격막 복원, 위장관 수술을 시행하였다.

소아에서 발생한 대장의 염증성 질환에서 E-cadherin의 발현 (E-cadherin Expression in Colonic Epithelium of Various Colitis in Children)

  • 이나영;박도윤;박재홍
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • 제12권2호
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    • pp.177-182
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    • 2009
  • 목 적: 소아에서 다양한 원인에 의해 발생한 대장염에서 점막의 형태학적 변화와 세포 접합에 다양한 변화가 있으리라 예상되어 세포 간의 결합을 유지하는 E-cadherin의 변화를 살펴보았다. 방 법: 1998년 1월부터 2003년 8월까지 부산대학교병원 소아청소년과에서 하부 위장관 내시경술과 대장점막 조직 검사를 통해 대장염으로 진단된 39명을 대상으로 하였다. 파라핀 블록에서 면역조직화학염색법을 이용하여 E-cadherin의 세포 내 발현을 조사하였다. 주변의 정상 조직과 비교하여 E-cadherin의 발현이 동일한 강도와 양상을 가진 세포가 50% 이상인 경우를 정상으로 판정하였고, 발현이 정상인 세포가 50% 미만이거나 염색 분포의 이상이 있거나 전혀 염색되지 않은 경우를 이상으로 판정하였다. 결 과: 1) 본 연구에서 비특이성 대장염 15예(38.5%), 크론병 7예(17.9%), 감염성 대장염 5예(12.8%), 음식 단백 과민성 직결장염 5예(12.8%), 궤양성 대장염 3예(7.7%), Henoch-Schonlein purpura 대장염 2예(5.1%), 그외 베체트병, 허혈성 대장염 1예가 포함되었다. 2) 모든 종류의 대장염에서 상피세포 E-cadherin 발현 감소가 관찰되었으며, 77%의 대상 표본에서 E-cadherin 발현감소가 있었다. 3) 활동성 염증이 심한 부위에서 Ecadherin 발현 감소가 현저하였으며 병변부에서 떨어진 상피세포에서는 정상 발현을, 궤양 주위나 재생 상피가 있는 부위는 심한 발현 감소를 보였다. 결 론: 모든 종류의 염증성 대장 질환에서 E-cadherin 발현 감소가 있었다. 이러한 변화는 염증과 궤양이 있는 부위에서 상피세포 접합을 느슨하게 함으로써 상피세포의 재생을 위한 세포의 이동을 용이하게 하기 위한 작용이라고 판단된다.

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TNF-$\alpha$ 자극에 의한 U937 단핵구 세포의 HT29 대장 상피 세포 부착에 대한 Berberine의 PPAR$\gamma$가 아닌 NF-$\kappa$B 경로를 통한 억제 효과 (Inhibitory Effect of Berberine on TNF-$\alpha$-induced U937 Monocytic Cell Adhesion to HT29 Human Colon Epithelial Cells is Mediated through NF-$\kappa$B Rather than PPAR$\gamma$)

  • 박수영;이광익;김일엽;김정애
    • 약학회지
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    • 제54권2호
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    • pp.91-96
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    • 2010
  • Berberine, an isoquinoline alkaloid, has a wide range of pharmacological effects, including anti-inflammation. It has been reported that berberine inhibits experimental colitis through inhibition of IL-8, and that inhibitory effect of berberine on inflammatory cytokine expression is mediated through peroxisome proliferator activated receptor (PPAR)-$\gamma$. In this study, we examined the effects and action mechanism of berberine on the tumor necrosis factor (TNF)-$\alpha$-induced monocyte adhesion to HT29 human colonic epithelial cells, which is commonly used as an in vitro model of inflammatory bowel disease (IBD). Berberine significantly inhibited the TNF-$\alpha$-induced monocyte adhesion to HT29, which is similar to the effect of PDTC, a nuclear factor (NF)-$\kappa$B inhibitor. However, ciglitazone and GW, the ligands of PPAR-$\gamma$, did not suppress the TNF-$\alpha$-induced monocyte adhesion to HT29 cells. In addition, TNF-$\alpha$-induced chemokine expression and NF-$\kappa$B transcriptional activity were significantly inhibited by berberine in a concentration-dependent manner. The results suggest that inhibitory effect of berberine on colitis is mediated through suppression of NF-$\kappa$B and NF-$\kappa$B-dependent chemokine expression.

Homozygous Missense Epithelial Cell Adhesion Molecule Variant in a Patient with Congenital Tufting Enteropathy and Literature Review

  • Guvenoglu, Merve;Simsek-Kiper, Pelin Ozlem;Kosukcu, Can;Taskiran, Ekim Z.;Saltik-Temizel, Inci Nur;Gucer, Safak;Utine, Eda;Boduroglu, Koray
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • 제25권6호
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    • pp.441-452
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    • 2022
  • Congenital diarrheal disorders (CDDs) with genetic etiology are uncommon hereditary intestinal diseases characterized by chronic, life-threatening, intractable watery diarrhea that starts in infancy. CDDs can be mechanistically divided into osmotic and secretory diarrhea. Congenital tufting enteropathy (CTE), also known as intestinal epithelial dysplasia, is a type of secretory CDD. CTE is a rare autosomal recessive enteropathy that presents with intractable neonatal-onset diarrhea, intestinal failure, severe malnutrition, and parenteral nutrition dependence. Villous atrophy of the intestinal epithelium, crypt hyperplasia, and irregularity of surface enterocytes are the specific pathological findings of CTE. The small intestine and occasionally the colonic mucosa include focal epithelial tufts. In 2008, Sivagnanam et al. discovered that mutations in the epithelial cell adhesion molecule (EpCAM, MIM# 185535) were the genetic cause of CTE (MIM# 613217). More than a hundred mutations have been reported to date. Furthermore, mutations in the serine peptidase inhibitor Kunitz type 2 (SPINT2, MIM# 605124) have been linked to syndromic CTE. In this study, we report the case of a 17-month-old male infant with congenital diarrhea. Despite extensive etiological workup, no etiology could be established before admission to our center. The patient died 15 hours after being admitted to our center in a metabolically decompensated state, probably due to a delay in admission and diagnosis. Molecular autopsy with exome sequencing revealed a previously reported homozygous missense variant, c.757G>A, in EpCAM, which was confirmed by histopathological examination.

대장유리피판(Colon Free Flap)을 이용한 식도재건의 구제술 (Salvage of Esophageal Reconstruction with Colon Free Flap)

  • 이상우;민경원
    • Archives of Plastic Surgery
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    • 제33권2호
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    • pp.245-248
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    • 2006
  • Besides gastric pull-up or colonic interposition, microvascular technique in esophageal reconstruction has been approved reliable methods. When free intestinal transfer is considered, jejunal free flap is commonly used. We treated the patient who had undergone reconstruction with a right colon interposition and suffered from inability of swallowing because of stricture and necrosis of the interposed flap. Although we have planned jejunal free transfer, we couldn't use jejunum due to adhesion by previous gastrojejunostomy and colon interposition. Salvage procedure with microvascualr free left colon flap was executed successfully. After 9 month follow-up, the patient was able to consume a normal diet.

Expression Patterns of Cancer Stem Cell Markers During Specific Celecoxib Therapy in Multistep Rat Colon Carcinogenesis Bioassays

  • Salim, Elsayed I;Hegazi, Mona M;Kang, Jin Seok;Helmy, Hager M
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권3호
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    • pp.1023-1035
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    • 2016
  • The purpose of this study was to investigate the role of colon cancer stem cells (CSCs) during chemically-induced rat multi-step colon carcinogenesis with or without the treatment with a specific cyclooxygenase-2 inhibitor drug (celecoxib). Two experiments were performed, the first, a short term 12 week colon carcinogenesis bioassay in which only surrogate markers for colon cancer, aberrant crypt foci (ACF) lesions, were formed. The other experiment was a medium term colon cancer rat assay in which tumors had developed after 32 weeks. Treatment with celecoxib lowered the numbers of ACF, as well as the tumor volumes and multiplicities after 32 weeks. Immunohistochemical proliferating cell nuclear antigen (PCNA) labeling indexes LI (%) were downregulated after treatment by celecoxib. Also different cell surface antigens known to associate with CSCs such as the epithelial cell adhesion molecule (EpCAM), CD44 and CD133 were compared between the two experiments and showed differential expression patterns depending on the stage of carcinogenesis and treatment with celecoxib. Flow cytometric analysis demonstrated that the numbers of CD133 cells were increased in the colonic epithelium after 12 weeks while those of CD44 but not CD133 cells were increased after 32 weeks. Moreover, aldehyde dehydrogenase-1 activity levels in the colonic epithelium (a known CSC marker) detected by ELISA assay were found down-regulated after 12 weeks, but were up-regulated after 32 weeks. The data have also shown that the protective effect of celecoxib on these specific markers and populations of CSCs and on other molecular processes such as apoptosis targeted by this drug may vary depending on the genetic and phenotypic stages of carcinogenesis. Therefore, uncovering these distinction roles of CSCs during different phases of carcinogenesis and during specific treatment could be useful for targeted therapy.