• 제목/요약/키워드: Tight-junction

검색결과 149건 처리시간 0.025초

Curcumin protects against the intestinal ischemia-reperfusion injury: involvement of the tight junction protein ZO-1 and TNF-α related mechanism

  • Tian, Shuying;Guo, Ruixue;Wei, Sichen;Kong, Yu;Wei, Xinliang;Wang, Weiwei;Shi, Xiaomeng;Jiang, Hongyu
    • The Korean Journal of Physiology and Pharmacology
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    • 제20권2호
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    • pp.147-152
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    • 2016
  • Present study aimed to investigate the effect of curcumin-pretreatment on intestinal I/R injury and on intestinal mucosa barrier. Thirty Wistar rats were randomly divided into: sham, I/R, and curcumin groups (n=10). Animals in curcumin group were pretreated with curcumin by gastric gavage (200 mg/kg) for 2 days before I/R. Small intestine tissues were prepared for Haematoxylin & Eosin (H&E) staining. Serum diamine oxidase (DAO) and tumor necrosis factor (TNF)-${\alpha}$ levels were measured. Expression of intestinal TNF-${\alpha}$ and tight junction protein (ZO-1) proteins was detected by Western blot and/or immunohistochemistry. Serum DAO level and serum and intestinal TNF-${\alpha}$ leves were significantly increased after I/R, and the values were markedly reduced by curcumin pretreatment although still higher than that of sham group (p<0.05 or p<0.001). H&E staining showed the significant injury to intestinal mucosa following I/R, and curcumin pretreatment significantly improved the histological structure of intestinal mucosa. I/R insult also induced significantly down-regulated expression of ZO-1, and the effect was dramatically attenuated by curcumin-pretreatment. Curcumin may protect the intestine from I/R injury through restoration of the epithelial structure, promotion of the recovery of intestinal permeability, as well as enhancement of ZO-1 protein expression, and this effect may be partly attributed to the TNF-${\alpha}$ related pathway.

Expression of Tight Junction Molecule In The Human Serum-Induced Aggregation of Human Abdominal Adipose-Derived Stem Cells In Vitro

  • Yoon, A Young;Yun, Sujin;Yang, HyeJin;Lim, Yoon Hwa;Kim, Haekwon
    • 한국발생생물학회지:발생과생식
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    • 제18권4호
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    • pp.213-224
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    • 2014
  • Previously we have shown that human abdominal adipose derived-stem cells (ADSCs) could aggregate during the high-density culture in the presence of human serum (HS). In the present study, we observed that human cord blood serum (CBS) and follicular fluid (HFF) also induced aggregation. Similarly, porcine serum could induce aggregation whereas bovine and sheep sera induced little aggregation. qRT-PCR analyses demonstrated that, compared to FBS-cultured ADSCs, HS-cultured cells exhibited higher level of mRNA expression of CLDN3, -6, -7, -15, and -16 genes among the tight junction proteins. ADSCs examined at the time of aggregation by culture with HS, BSA, HFF, CBS, or porcine serum showed significantly higher level of mRNA expression of JAM2 among JAM family members. In contrast, cells cultured in FBS, bovine serum or sheep serum, showed lower level of JAM2 expression. Immunocytochemical analyses demonstrated that the aggregates of HS-cultured cells (HS-Agg) showed intense staining against the anti-JAM2 antibody whereas neither non-aggregated cells (HS-Ex) nor FBS-cultured cells exhibited weak staining. Western blot results showed that HS-Agg expressed JAM2 protein more prominently than HS-Ex and FBS-cultured cells, both of latter reveled weaker intensity. These results suggest that the aggregation property of ADSCs during high-density culture would be dependent on the specific components of serum, and that JAM2 molecule could play a role in the animal sera-induced aggregation in vitro.

미네랄워터의 피부 장벽 보호 효과 연구 (The Protective Effect of Mineral Water Against UVB Irradiation)

  • 이성훈;민대진;나용주;심종원;권이경;조준철;이해광
    • 대한화장품학회지
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    • 제39권1호
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    • pp.39-46
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    • 2013
  • 칼슘, 마그네슘과 같은 양이온은 피부 장벽을 보호하는 기능이 있다고 알려져 있다. 본 연구의 목적은 칼슘, 마그네슘, 망간, 불소로 이루어진 미네랄워터의 피부 장벽 보호 기능을 확인하기 위한 것이다. 피부가 자외선에 노출되게 되면 밀착연접(tight junction, TJ)이 파괴되며, 밀착연접으로 이루어진 피부 장벽도 손상 받게된다. 미네랄워터가 자외선에 의해 손상된 피부의 장벽기능을 보호할 수 있는지 평가하기 위해 인공피부 모델을 이용한 실험을 진행하였다. 인공피부에 자외선을 조사하고 미네랄워터를 처리하면 피부 장벽 손상을 막아준다. TJ permeability assay를 통하여 자외선 처리 시 손상된 밀착연접 장벽이 미네랄워터 처리에 의해 유지되는 것을 확인하였다. 각질형성세포를 이용한 실험에서 미네랄워터가 밀착연접 구조를 유지시켜 주고, 자외선에 의해 감소된 occludin 단백질의 생성량이 회복되는 것을 확인하였다. 따라서 본 연구를 통해 미네랄워터는 자외선에 의한 피부 장벽 파괴를 막아주는 효과가 있음을 확인할 수 있었다.

만성 역류성 식도염에서 황련과 오수유 혼합물이 식도 점막에 미치는 효과 (Effect of Coptidis Rhizoma and Evodiae Fructus Mixture on Esophageal Mucosa in Chronic Reflux Esophagitis)

  • 이진아;신미래;이지혜;노성수
    • 생약학회지
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    • 제51권4호
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    • pp.349-359
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    • 2020
  • Gastroesophageal reflux disease (GERD) is a disease that stomach contents continually refluxing, and is currently on the rise worldwide. The purpose of this study is to find natural materials that can reduce side effects and effectively treat chronic acid reflux esophagitis (CARE), one of GERD. First, the antioxidant activity was confirmed by varying the mixing ratio of Coptidis Rhizoma and Evodiae Fructus, which are effective against chronic reflux esophagitis. After, animal experiments were conducted using a 1:1 (CE) and 1:2 (CEE) combination ratio of Coptidis Rhizoma and Evodiae Fructus, which had the best antioxidant efficacy. Gross lesion of esophageal mucosa after CE or CEE treatment showed a superior enhancement compared with that of CARE control rats. Additionally, its inhibited MAPK phosphorylation and led NF-κB inactivation through the suppression of IκBα phosporylation by regulating Nrf2/Keap-1, and NF-κB inactivation induced reduced protein expressions including inflammatory mediators and cytokines. Moreover, its improved esophageal barrier function through upregulating protein expressions of tight junction protein, whereas downregulating protein expressions of MMPs. Taken together, a mixture of Coptidis Rhizoma and Evodiae Fructus can attenuate the esophageal mucosal ulcer by inhibiting MAPK and NF-κB pathway, and upregulating proteins associated with tight junction.

왕우렁이 추출물의 역류성 식도염 억제 효과 (The Anti-inflammatory Effects of Golden Apple Snail (Pomacea canaliculata) in Reflux Esophagitis Model)

  • 남현화;류승목;양선규;김욱진;문병철;서윤수
    • 한국유기농업학회지
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    • 제29권1호
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    • pp.85-96
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    • 2021
  • 본 결과를 통해, 왕우렁이 추출물의 역류성 식도염 모델에서 위 내용물의 역류로 인한 조직손상에 대한 보호효과를 확인하였다. 식도 점막의 육안 소견과 조직병리학적 분석 결과 점막의 괴사, 염증세포의 침윤 등의 증상이 완화됨을 확인하였으며, 상피조직의 tight junction을 보호하여 위산과 펩신으로부터 점막을 보호하는 것을 확인하였다. 이러한 왕우렁이 추출물의 식도 보호효과는 NF-κB 기전의 조절을 통해 점막의 염증반응을 억제하여 나타나는 것으로 생각된다. 이상의 결과를 종합하였을 때, 왕우렁이 추출물이 역류성 식도염 완화를 위한 기능성 소재로서의 가능성을 가지는 것으로 사료된다.

Phosphorylation of tyrosine-14 on Caveolin-1 enhances lipopolysaccharide-induced inflammation in human intestinal Caco-2 cells

  • Gong Deuk Bae;Kyong Kim;Se-Eun Jang;Dong-Jae Baek;Eun-Young Park;Yoon Sin Oh
    • Journal of Applied Biological Chemistry
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    • 제66권
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    • pp.311-319
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    • 2023
  • Caveolin-1 (Cav-1) is the main structural component of the caveolae on the plasma membrane, which regulates various cellular processes, including cell growth, differentiation, and endocytosis. Although a recent study demonstrated that Cav-1 might be involved in diabetes-associated inflammation, its exact role in the intestine was unclear. In this study, we examined the intestinal expression of Cav-1 in diabetic conditions. We also investigated its effect on lipopolysaccharide (LPS)-induced inflammation by expressing this protein in human intestinal Caco-2 cells lacking Cav-1. We observed that increased Cav-1 levels and decreased expression of tight junction proteins affected intestinal permeability in high-fat diet-induced diabetic mice. When Caco-2 cells were treated with LPS, Cav-1 enhanced the NF-κB signaling. Moreover, LPS reduced the expression of tight junction proteins while it increased cell-cell permeability and reactive oxygen species generation in Caco-2 cells and this effect was amplified by cav-1 overexpression. LPS treatment promoted phosphorylation of tyrosine-14 (Y14) on Cav-1, and the LPS-induced NF-κB signaling was suppressed in cells expressing non-phosphorylatable Cav-1 (tyrosine-14 to phenylalanine mutant), which reduced intestinal barrier permeability. These results suggest that Cav-1 expression promotes LPS-induced inflammation in Caco-2 cells, and phosphorylation of Y14 on Cav-1 might contribute to the anti-inflammatory response in LPS-induced NF-κB signaling and cell permeability.

Lactic Acid Bacteria Improves Peyer's Patch Cell-Mediated Immunoglobulin A and Tight-Junction Expression in a Destructed Gut Microbial Environment

  • Kim, Sung Hwan;Jeung, Woonhee;Choi, Il-Dong;Jeong, Ji-Woong;Lee, Dong Eun;Huh, Chul-Sung;Kim, Geun-Bae;Hong, Seong Soo;Shim, Jae-Jung;Lee, Jung Lyoul;Sim, Jae-Hun;Ahn, Young-Tae
    • Journal of Microbiology and Biotechnology
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    • 제26권6호
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    • pp.1035-1045
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    • 2016
  • To evaluate the effects of lactic acid bacteria (LAB) on Peyer's patch cells, mice were treated with a high dose of kanamycin to disturb the gut microbial environment. The overarching goal was to explore the potential of LAB for use as a dietary probiotic that buffers the negative consequences of antibiotic treatment. In vitro, LAB stimulated the production of immunoglobulin A (IgA) from isolated Peyer's patch cells. Inflammation-related genes (TNF-α, IL-1β, and IL-8) were up-regulated in Caco-2 cells stimulated with lipopolysaccharide (LPS), while tight-junction-related genes (ZO-1 and occludin) were down-regulated; the effects of LPS on inflammatory gene and tight-junction gene expression were reversed by treatment with LAB. Mice treated with a high dose of kanamycin showed increased serum IgE levels and decreases in serum IgA and fecal IgA levels; the number of Peyer's patch cells decreased with kanamycin treatment. However, subsequent LAB treatment was effective in reducing the serum IgE level and recovering the serum IgA and fecal IgA levels, as well as the number of Peyer's patch cells. In addition, ZO-1 and occludin mRNA levels were up-regulated in the ileum tissues of mice receiving LAB treatment. Lactic acid bacteria can enhance the intestinal immune system by improving the integrity of the intestinal barrier and increasing the production of IgA in Peyer's patches. Lactic acid bacteria should be considered a potential probiotic candidate for improving intestinal immunity, particularly in mitigating the negative consequences of antibiotic use.

인체유방암세포의 tight junction 기능 조절을 통한 genistein의 암세포 침윤 억제 효과 (Anti-invasive Activity of Human Breast Carcinoma Cells by Genistein through Modulation of Tight Junction Function)

  • 김성옥;정영기;최영현
    • 생명과학회지
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    • 제19권9호
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    • pp.1200-1208
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    • 2009
  • Tight junctions (TJs)은 인접된 세포 사이의 전해질 및 거대분자 확산 조절에 관여하는 paracellular permeability의 장벽 역할을 한다. 본 연구에서는 MCF-7 및 MDA-MB-231 인체유방암세포에서 대두의 대표적인 생리활성물인 genistein에 의한 암세포의 침윤 억제에서 TJs의 견고성 및 투과성과의 연관성을 조사하였다. 본 연구의 결과에 의하면 genistein에 의한 유방암세포의 증식 억제, 암세포 이동성의 저하 및 침윤성의 억제는 TJs의 증가된 견고성과 연관이 있었으며, 이를 transepithelial electrical resistance의 증가 및 paracellular permeability의 감소로 확인하였다. Genistein은 두 유방암세포에서 TJs의 주요 조절 단백질로서 paracellular transport 조절에 중요한 역할을 하는 claudin-3 및 claudin-4의 발현을 억제시켰다. 그리고 genistein은 암세포의 전이 조절 관련 유전자들인 like growth factor-1 receptor 및 snail의 발현을 억제하였으며, thrombospondin-1 및 E-cadherin의 발현은 증가시켰다. 또한 small interfering RNA를 이용하여 genistein의 유방암세포의 침윤 억제에서 claudin-3단백질의 중요성을 확인하였다. 결론적으로 genistein이 TJs의 견고성 증가를 통하여 암세포의 침윤성을 억제할 수 있었으며, 이 과정에서 아마도 claudin 단백질의 발현 증가가 중요한 역할을 하고 있음을 알 수 있었다. 본 연구의 결과는 genistein이 종양 전이억제를 효과적으로 차단할 수 있음을 보여주는 것이다.

Effects of multi-strain probiotic supplementation on intestinal microbiota, tight junctions, and inflammation in young broiler chickens challenged with Salmonella enterica subsp. enterica

  • Chang, Chi Huan;Teng, Po Yun;Lee, Tzu Tai;Yu, Bi
    • Asian-Australasian Journal of Animal Sciences
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    • 제33권11호
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    • pp.1797-1808
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    • 2020
  • Objective: This study assessed the effects of probiotics on cecal microbiota, gene expression of intestinal tight junction proteins, and immune response in the cecal tonsil of broiler chickens challenged with Salmonella enterica subsp. enterica. Methods: One-day-old broiler chickens (n = 240) were randomly allocated to four treatments: negative control (Cont), multi-strain probiotic-treated group (Pro), Salmonella-infected group (Sal), and multi-strain probiotic-treated and Salmonella-infected group (ProSal). All chickens except those in the Cont and Pro groups were gavaged with 1×108 cfu/mL of S. enterica subsp. enterica 4 days after hatching. Results: Our results indicated that body weight, weight gain, and feed conversion ratio of birds were significantly reduced (p<0.05) by Salmonella challenge. Chickens challenged with Salmonella decreased cecal microbial diversity. Chickens in the Sal group exhibited abundant Proteobacteria than those in the Cont, Pro, and ProSal groups. Salmonella infection downregulated gene expression of Occludin, zonula occludens-1 (ZO1), and Mucin 2 in the jejunum and Occludin and Claudin in the ileum. Moreover, the Sal group increased gene expression of interferon-γ (IFN-γ), interleukin-6 (IL-6), IL-1β, and lipopolysaccharide-induced tumor necrosis factor-alpha factor (LITAF) and reduced levels of transforming growth factor-β4 and IL-10 compared with the other groups (p<0.05). However, chickens receiving probiotic diets increased Lactobacillaceae abundance and reduced Enterobacteriaceae abundance in the ceca. Moreover, supplementation with probiotics increased the mRNA expression of Occludin, ZO1, and Mucin 2 in the ileum (p<0.05). In addition, probiotic supplementation downregulated the mRNA levels of IFN-γ (p<0.05) and LITAF (p = 0.075) and upregulated IL-10 (p = 0.084) expression in the cecal tonsil. Conclusion: The administration of multi-strain probiotics modulated intestinal microbiota, gene expression of tight junction proteins, and immunomodulatory activity in broiler chickens.

Immunofluorescence Microscopic Evaluation of Tight Junctional Proteins during Enterotoxigenic Bacteroides fragilis (ETBF) Infection in Mice

  • Hwang, Soonjae;Kang, Yeowool;Jo, Minjeong;Kim, Sung Hoon;Cho, Won Gil;Rhee, Ki-Jong
    • 대한의생명과학회지
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    • 제24권3호
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    • pp.275-279
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    • 2018
  • Inflammatory bowel disease (IBD) is increasing in prevalence in developed countries but the cause of this increase is unclear. In animal models of IBD and in human IBD patients, alterations in the tight junctional proteins have been observed, suggesting that the intestinal microflora may penetrate the underlying colonic tissue and promote inflammation. Enterotoxigenic Bacteroides fragilis (ETBF) causes inflammatory diarrhea in human and is implicated in inflammatory bowel diseases. However, it is unclear whether alterations in tight junctional proteins occur during ETBF infection in mice. In this brief communication, we report that ETBF infection induces up-regulation of claudin-2 and down-regulation of claudin-5 through B. fragilis toxin (BFT) activity in the large intestine of C57BL/6 mice. In contrast, BFT did not induce changes in tight junctional proteins in the HT29/C1 cell line, suggesting that analysis of biological activity of BFT in vivo is important for evaluating ETBF effects.