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  1. AU="Yu, Mo-Sang"
  2. AU="Arshad, Hassaan Bin"
  3. AU="Schwänke, Ulf"
  4. AU=Martin Rick
  5. AU="Narges ROUSTAEI"
  6. AU="Alsaady, Ammar"
  7. AU=Guo Zhinian
  8. AU=Dho Sascha E
  9. AU="Santiso-Quiñones, Gustavo"
  10. AU="Donovan, Lois E"
  11. AU="Xiong, Zhuo-Chao"
  12. AU="Mu, Dezhi"
  13. AU="Kaiser, Steffen"
  14. AU=Garlepp M J
  15. AU=Yang Zhenwei
  16. AU="Guillot, Loic"
  17. AU=Pocrnic Ivan
  18. AU="Rackova, Sylva"
  19. AU="Jordan Denizeau"
  20. AU="Alexandra J. Corbett"
  21. AU="Felderman, Howard E"
  22. AU="Chen, Fuxing"
  23. AU="Soekadar, Surjo R"
  24. AU="Pagotto, Sara"
  25. AU="Dominguez, Georgina Cutillas"
  26. AU=Barabutis Nektarios
  27. AU="Rumalla, Kavelin"
  28. AU=Meares Gordon P.
  29. AU="Gawron, Lori M"
  30. AU=Guettari Moez
  31. AU=Ma Xingcong
  32. AU="Greene, Kerrie" AU="Greene, Kerrie"
  33. AU="Adebayo, Abe"
  34. AU=Amoako Yaw Ampem
  35. AU="Khanna, Sakshum"

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  1. Artikel ; Online: Resveratrol alleviates intestinal mucosal barrier dysfunction in dextran sulfate sodium-induced colitis mice by enhancing autophagy.

    Pan, Hang-Hai / Zhou, Xin-Xin / Ma, Ying-Yu / Pan, Wen-Sheng / Zhao, Fei / Yu, Mo-Sang / Liu, Jing-Quan

    World journal of gastroenterology

    2020  Band 26, Heft 33, Seite(n) 4945–4959

    Abstract: Background: Intestinal mucosal barrier dysfunction plays an important role in the pathogenesis of ulcerative colitis (UC). Recent studies have revealed that impaired autophagy is associated with intestinal mucosal dysfunction in the mucosa of colitis ... ...

    Abstract Background: Intestinal mucosal barrier dysfunction plays an important role in the pathogenesis of ulcerative colitis (UC). Recent studies have revealed that impaired autophagy is associated with intestinal mucosal dysfunction in the mucosa of colitis mice. Resveratrol exerts anti-inflammatory functions by regulating autophagy.
    Aim: To investigate the effect and mechanism of resveratrol on protecting the integrity of the intestinal mucosal barrier and anti-inflammation in dextran sulfate sodium (DSS)-induced ulcerative colitis mice.
    Methods: Male C57BL/6 mice were divided into four groups: negative control group, DSS model group, DSS + resveratrol group, and DSS + 5-aminosalicylic acid group. The severity of colitis was assessed by the disease activity index, serum inflammatory cytokines were detected by enzyme-linked immunosorbent assay. Colon tissues were stained with haematoxylin and eosin, and mucosal damage was evaluated by mean histological score. The expression of occludin and ZO-1 in colon tissue was evaluated using immunohistochemical analysis. In addition, the expression of autophagy-related genes was determined using reverse transcription-polymerase chain reaction and Western-blot, and morphology of autophagy was observed by transmission electron microscopy.
    Results: The resveratrol treatment group showed a 1.72-fold decrease in disease activity index scores and 1.42, 3.81, and 1.65-fold decrease in the production of the inflammatory cytokine tumor necrosis factor-α, interleukin-6 and interleukin-1β, respectively, in DSS-induced colitis mice compared with DSS group (
    Conclusion: Resveratrol treatment decreased the expression of inflammatory factors, increased the expression of tight junction proteins and alleviated UC intestinal mucosal barrier dysfunction; this effect may be achieved by enhancing autophagy in intestinal epithelial cells.
    Mesh-Begriff(e) Animals ; Autophagy ; Colitis/chemically induced ; Colitis/drug therapy ; Colon ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Intestinal Mucosa ; Male ; Mice ; Mice, Inbred C57BL ; Resveratrol/pharmacology
    Chemische Substanzen Dextran Sulfate (9042-14-2) ; Resveratrol (Q369O8926L)
    Sprache Englisch
    Erscheinungsdatum 2020-09-20
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v26.i33.4945
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: MiR-30e-UCP2 pathway regulates alcoholic hepatitis progress by influencing ATP and hydrogen peroxide expression.

    Jin, Xi / Yu, Mo-Sang / Huang, Yue / Xiang, Zun / Chen, Yi-Peng

    Oncotarget

    2017  Band 8, Heft 38, Seite(n) 64294–64302

    Abstract: To investigate the expression of miR-30e-UCP2 pathway in different stages of alcoholic liver disease (ALD) and its capacity and mechanism in regulating alcoholic hepatitis (AH) progress. C57BL/6 mice were fed with Lieber-DeCaril (LD) diet for 4 and 12 ... ...

    Abstract To investigate the expression of miR-30e-UCP2 pathway in different stages of alcoholic liver disease (ALD) and its capacity and mechanism in regulating alcoholic hepatitis (AH) progress. C57BL/6 mice were fed with Lieber-DeCaril (LD) diet for 4 and 12 weeks to establish models of alcoholic fat infiltration (AFI) and AH. Based on AFI feeding, the alcoholic hepatic fibrosis (AHF) was set up with additional 4 weeks 5% carbon tetrachloride intra-abdominal injection twice per week. Serum lipid and inflammation related makers were detected while H-E staining for hepatic steatosis/ inflammation and Sirius staining for hepatic fibrosis were conducted. The apoptosis degree was tested by TUNEL plot while the hydrogen peroxide (H
    Sprache Englisch
    Erscheinungsdatum 2017-09-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.19729
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis.

    Ren, Meng-Ting / Gu, Meng-Li / Zhou, Xin-Xin / Yu, Mo-Sang / Pan, Hang-Hai / Ji, Feng / Ding, Chen-Yan

    World journal of gastroenterology

    2019  Band 25, Heft 38, Seite(n) 5800–5813

    Abstract: Background: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD: Aim: To investigate the role of SIRT1 in intestinal epithelial cells (IECs) in UC and further explore the underlying mechanisms.: Methods: We developed a coculture model ... ...

    Abstract Background: Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD
    Aim: To investigate the role of SIRT1 in intestinal epithelial cells (IECs) in UC and further explore the underlying mechanisms.
    Methods: We developed a coculture model using macrophages and Caco-2 cells. After treatment with the SIRT1 activator SRT1720 or inhibitor nicotinamide (NAM), the expression of occludin and zona occludens 1 (ZO-1) was assessed by Western blot analysis. Annexin V-APC/7-AAD assays were performed to evaluate Caco-2 apoptosis. Dextran sodium sulfate (DSS)-induced colitis mice were exposed to SRT1720 or NAM for 7 d. Transferase-mediated dUTP nick-end labeling (TUNEL) assays were conducted to assess apoptosis in colon tissues. The expression levels of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, caspase-9, and caspase-3 in Caco-2 cells and the colon tissues of treated mice were examined by quantitative real-time PCR and Western blot.
    Results: SRT1720 treatment increased the protein levels of occludin and ZO-1 and inhibited Caco-2 apoptosis, whereas NAM administration caused the opposite effects. DSS-induced colitis mice treated with SRT1720 had a lower disease activity index (
    Conclusion: SIRT1 activation reduces apoptosis of IECs
    Mesh-Begriff(e) Animals ; Apoptosis ; Caco-2 Cells ; Caspase 12/metabolism ; Coculture Techniques ; Colitis, Ulcerative/chemically induced ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/pathology ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Endoplasmic Reticulum Stress ; Epithelial Cells/drug effects ; Epithelial Cells/pathology ; Female ; Heterocyclic Compounds, 4 or More Rings/administration & dosage ; Humans ; Intestinal Mucosa/cytology ; Intestinal Mucosa/pathology ; Macrophages ; Mice ; Niacinamide/administration & dosage ; Sirtuin 1/antagonists & inhibitors ; Sirtuin 1/metabolism ; Transcription Factor CHOP/metabolism
    Chemische Substanzen DDIT3 protein, human ; Heterocyclic Compounds, 4 or More Rings ; SRT1720 ; Transcription Factor CHOP (147336-12-7) ; Niacinamide (25X51I8RD4) ; Dextran Sulfate (9042-14-2) ; CASP12 protein, human (EC 3.4.22.-) ; Casp12 protein, mouse (EC 3.4.22.-) ; Caspase 12 (EC 3.4.22.-) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
    Sprache Englisch
    Erscheinungsdatum 2019-09-30
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v25.i38.5800
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Mesh migration into the sigmoid colon after inguinal hernia repair presenting as a colonic polyp: A case report and review of literature.

    Liu, Sha / Zhou, Xin-Xin / Li, Lin / Yu, Mo-Sang / Zhang, Hong / Zhong, Wei-Xiang / Ji, Feng

    World journal of clinical cases

    2018  Band 6, Heft 12, Seite(n) 564–569

    Abstract: Mesh migration and penetration into abdominal viscera rarely occur after laparoscopic inguinal hernia repair. We present the first case of mesh migration into the sigmoid colon identified as a colonic polyp at initial colonoscopic examination. The ... ...

    Abstract Mesh migration and penetration into abdominal viscera rarely occur after laparoscopic inguinal hernia repair. We present the first case of mesh migration into the sigmoid colon identified as a colonic polyp at initial colonoscopic examination. The patient complained of mild abdominal distention in the lower abdomen over the previous year without changes in bowel habits or stool appearance and without weight loss. By complementary endoscopic ultrasonography, a cavity-like structure beneath the suspected polyp was further confirmed. Enhanced abdominal computed tomography merely revealed local bowel wall thickening and inflammation of the colosigmoid junction. The migrating mesh, which was lodged in the sigmoid colon and caused intra-abdominal adhesion in the lower abdominal cavity, was finally identified via exploratory surgery. The components of inflammatory granulation tissue around the mesh material were diagnosed based on histological examination of the surgical specimen after sigmoidectomy. In this patient, nonspecific endoscopic and imaging outcomes during clinical work-up led to the diagnostic dilemma of mesh migration. Therefore, the clinical, radiological and endoscopic challenges specific to this case as well as the underlying reasons for mesh migration are discussed in detail.
    Sprache Englisch
    Erscheinungsdatum 2018-10-31
    Erscheinungsland United States
    Dokumenttyp Case Reports
    ISSN 2307-8960
    ISSN 2307-8960
    DOI 10.12998/wjcc.v6.i12.564
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Sigmoid colon translocation of an intrauterine device misdiagnosed as a colonic polyp: A case report.

    Zhou, Xin-Xin / Yu, Mo-Sang / Gu, Meng-Li / Zhong, Wei-Xiang / Wu, Hong-Ru / Ji, Feng / Pan, Hang-Hai

    Medicine

    2018  Band 97, Heft 6, Seite(n) e9840

    Abstract: Rationale: Intrauterine contraceptive devices (IUDs) are recommended as a means of contraception. Translocation of IUD is a rare and serious complication. Colonic inflammatory mass caused by translocated IUD initially misdiagnosed as a colonic polyp is ... ...

    Abstract Rationale: Intrauterine contraceptive devices (IUDs) are recommended as a means of contraception. Translocation of IUD is a rare and serious complication. Colonic inflammatory mass caused by translocated IUD initially misdiagnosed as a colonic polyp is extremely rare and has not been reported yet.
    Patient concerns: This report presents a case of sigmoid colon translocation of intrauterine device on a 37-year-old female patient. Colonoscopy was performed due to her complain of repeated blood in stools and subsequently the patient was misdiagnosed as a sigmoid colon polyp. Nonetheless, the "polyp" was not able to be removed endoscopically.
    Diagnoses: Sigmoid colon translocation of an intrauterine device.
    Interventions: To further clarify the diagnosis, computed tomography (CT) scan was performed and the "polyp" was confirmed to be caused by a translocated IUD.
    Outcomes: The translocated IUD was removed easily by surgery, and the patient recovered soon after the operation.
    Lessons: The present case indicates that an annual gynaecologic examination is necessary to determine the position of the IUD, and a CT examination may help confirm an ectopic IUD.
    Mesh-Begriff(e) Adult ; Colitis/diagnosis ; Colitis/etiology ; Colitis/surgery ; Colon, Sigmoid/pathology ; Colon, Sigmoid/surgery ; Colonic Polyps/diagnosis ; Colonoscopy/methods ; Device Removal/methods ; Diagnosis, Differential ; Diagnostic Errors ; Female ; Humans ; Intrauterine Device Migration/adverse effects ; Intrauterine Devices/adverse effects ; Tomography, X-Ray Computed/methods ; Treatment Outcome
    Sprache Englisch
    Erscheinungsdatum 2018-01-09
    Erscheinungsland United States
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 80184-7
    ISSN 1536-5964 ; 0025-7974
    ISSN (online) 1536-5964
    ISSN 0025-7974
    DOI 10.1097/MD.0000000000009840
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Blockage of ETS homologous factor inhibits the proliferation and invasion of gastric cancer cells through the c-Met pathway.

    Gu, Meng-Li / Zhou, Xin-Xin / Ren, Meng-Ting / Shi, Ke-Da / Yu, Mo-Sang / Jiao, Wen-Rui / Wang, Ya-Mei / Zhong, Wei-Xiang / Ji, Feng

    World journal of gastroenterology

    2020  Band 26, Heft 47, Seite(n) 7497–7512

    Abstract: Background: Gastric cancer (GC) is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency, but its exact pathogenesis has not been fully elucidated. ETS homologous factor (EHF) is an ... ...

    Abstract Background: Gastric cancer (GC) is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency, but its exact pathogenesis has not been fully elucidated. ETS homologous factor (EHF) is an important member of the ETS family and contributes to the pathogenesis of multiple malignant tumors. To date, whether EHF participates in the development of GC
    Aim: To investigate the role and mechanism of EHF in the occurrence and development of GC.
    Methods: The expression of EHF mRNA in GC tissues and cell lines was measured by quantitative PCR. Western blotting was performed to determine the protein expression of EHF, c-Met, and its downstream signal molecules. The EHF expression in GC tissues was further detected by immunohistochemical staining. To investigate the role of EHF in GC oncogenesis, small interfering RNA (siRNA) against EHF was transfected into GC cells. The cell proliferation of GC cells was determined by Cell Counting Kit-8 and colony formation assays. Flow cytometry was performed following Annexin V/propidium iodide (PI) to identify apoptotic cells and PI staining to analyze the cell cycle. Cell migration and invasion were assessed by transwell assays.
    Results: The data showed that EHF was upregulated in GC tissues and cell lines in which increased expression of c-Met was also observed. Silencing of EHF by siRNA reduced the proliferation of GC cells. Inhibition of EHF induced significant apoptosis and cell cycle arrest in GC cells. Cell migration and invasion were significantly inhibited. EHF silencing led to c-Met downregulation and further blocked the Ras/c-Raf/extracellular signal-related kinase 1/2 (Erk1/2) pathway. Additionally, phosphatase and tensin homolog was upregulated and glycogen synthase kinase 3 beta was deactivated. Moreover, inactivation of signal transducer and activator of transcription 3 was detected following EHF inhibition, leading to inhibition of the epithelial-to-mesenchymal transition (EMT).
    Conclusion: These results suggest that EHF plays a key role in cell proliferation, invasion, apoptosis, the cell cycle and EMT
    Mesh-Begriff(e) Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasm Invasiveness ; Stomach Neoplasms/genetics
    Sprache Englisch
    Erscheinungsdatum 2020-12-29
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v26.i47.7497
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  7. Artikel ; Online: Adipose-derived mesenchymal stem cells alleviate TNBS-induced colitis in rats by influencing intestinal epithelial cell regeneration, Wnt signaling, and T cell immunity.

    Gao, Jian-Guo / Yu, Mo-Sang / Zhang, Meng-Meng / Gu, Xue-Wei / Ren, Yue / Zhou, Xin-Xin / Chen, Dong / Yan, Tian-Lian / Li, You-Ming / Jin, Xi

    World journal of gastroenterology

    2020  Band 26, Heft 26, Seite(n) 3750–3766

    Abstract: Background: Conventional Crohn's disease (CD) treatments are supportive rather than curative and have serious side effects. Adipose-derived mesenchymal stem cells (ADSCs) have been gradually applied to treat various diseases. The therapeutic effect and ... ...

    Abstract Background: Conventional Crohn's disease (CD) treatments are supportive rather than curative and have serious side effects. Adipose-derived mesenchymal stem cells (ADSCs) have been gradually applied to treat various diseases. The therapeutic effect and underlying mechanism of ADSCs on CD are still not clear.
    Aim: To investigate the effect of ADSC administration on CD and explore the potential mechanisms.
    Methods: Wistar rats were administered with 2,4,6-trinitrobenzene sulfonic acid (TNBS) to establish a rat model of CD, followed by tail injections of green fluorescent protein (GFP)-modified ADSCs. Flow cytometry, qRT-PCR, and Western blot were used to detect changes in the Wnt signaling pathway, T cell subtypes, and their related cytokines.
    Results: The isolated cells showed the characteristics of ADSCs, including spindle-shaped morphology, high expression of CD29, CD44, and CD90, low expression of CD34 and CD45, and osteogenic/adipogenic ability. ADSC therapy markedly reduced disease activity index and ameliorated colitis severity in the TNBS-induced rat model of CD. Furthermore, serum anti-sacchromyces cerevisiae antibody and p-anti-neutrophil cytoplasmic antibody levels were significantly reduced in ADSC-treated rats. Mechanistically, the GFP-ADSCs were colocalized with intestinal epithelial cells (IECs) in the CD rat model. GFP-ADSC delivery significantly antagonized TNBS-induced increased canonical Wnt pathway expression, decreased noncanonical Wnt signaling pathway expression, and increased apoptosis rates and protein level of cleaved caspase-3 in rats. In addition, ADSCs attenuated TNBS-induced abnormal inflammatory cytokine production, disturbed T cell subtypes, and their related markers in rats.
    Conclusion: Successfully isolated ADSCs show therapeutic effects in CD by regulating IEC proliferation, the Wnt signaling pathway, and T cell immunity.
    Mesh-Begriff(e) Adipose Tissue ; Animals ; Colitis/chemically induced ; Colitis/therapy ; Epithelial Cells ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells ; Rats ; Rats, Wistar ; Regeneration ; T-Lymphocytes ; Trinitrobenzenesulfonic Acid/toxicity ; Wnt Signaling Pathway
    Chemische Substanzen Trinitrobenzenesulfonic Acid (8T3HQG2ZC4)
    Sprache Englisch
    Erscheinungsdatum 2020-08-09
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v26.i26.3750
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition.

    Ning, Jian-Wen / Zhang, Yan / Yu, Mo-Sang / Gu, Meng-Li / Xu, Jia / Usman, Ali / Ji, Feng

    Hepatobiliary & pancreatic diseases international : HBPD INT

    2017  Band 16, Heft 4, Seite(n) 431–436

    Abstract: Background: Emodin, a traditional Chinese medicine, has a therapeutic effect on severe acute pancreatitis (SAP), whereas the underlying mechanism is still unclear. Studies showed that the intestinal mucosa impairment, and subsequent release of endotoxin ...

    Abstract Background: Emodin, a traditional Chinese medicine, has a therapeutic effect on severe acute pancreatitis (SAP), whereas the underlying mechanism is still unclear. Studies showed that the intestinal mucosa impairment, and subsequent release of endotoxin and proinflammatory cytokines such as IL-1β, which further leads to the dysfunction of multiple organs, is the potentially lethal mechanism of SAP. Caspase-1, an IL-1β-converting enzyme, plays an important role in this cytokine cascade process. Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP.
    Methods: Eighty Sprague-Dawley rats were randomly divided into four groups (n=20 each group): SAP, sham-operated (SO), emodin-treated (EM) and caspase-1 inhibitor-treated (ICE-I) groups. SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct. Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction. Serum levels of IL-1β, IL-18 and endotoxin, histopathological alteration of pancreas tissues, intestinal mucosa, and the intestinal caspase-1 mRNA and protein expressions were assessed 24 hours after SAP induction.
    Results: Rats in the SAP group had higher serum levels of IL-1β and IL-18 (P<0.05), pancreatic and gut pathological scores (P<0.05), and caspase-1 mRNA and protein expressions (P<0.05) compared with the SO group. Compared with the SAP group, rats in the EM and ICE-I groups had lower IL-1β and IL-18 levels (P<0.05), lower pancreatic and gut pathological scores (P<0.05), and decreased expression of intestine caspase-1 mRNA (P<0.05). Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions, more disappeared intercellular joints, and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups.
    Conclusions: Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP. Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines, including IL-1β and IL-18. Our animal data may be applicable in clinical practice.
    Sprache Englisch
    Erscheinungsdatum 2017-08-15
    Erscheinungsland Singapore
    Dokumenttyp Journal Article
    ZDB-ID 2241386-8
    ISSN 1499-3872
    ISSN 1499-3872
    DOI 10.1016/S1499-3872(17)60041-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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