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Condition: Inflammatory Bowel Disease
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Total 147 results found since Jan 2013.
Effects of particle size and binding affinity for siRNA on the cellular processing, intestinal permeation, and anti‐inflammatory efficacy of polymeric nanoparticles
ConclusionNanoparticles with particle size of 450 nm or more balanced binding affinity for siRNA might be preferable for the treatment of ulcerative colitis. This article is protected by copyright. All rights reserved.
Source: The Journal of Gene Medicine - August 9, 2015 Category: Genetics & Stem Cells Authors: Wenyue Cheng, Cui Tang, Chunhua Yin Tags: Research Article Source Type: research
Heterogeneous Nuclear Ribonucleoprotein A1 Improves the Intestinal Injury by Regulating Apoptosis Through Trefoil Factor 2 in Mice with Anti-CD3–induced Enteritis
Conclusions: hnRNP A1 improves intestinal injury in anti-CD3 antibody–induced enteritis mice through the upregulation of TFF2, which regulates apoptosis and enhances epithelial restoration, whereas this molecule ameliorates DSS-induced colitis through a different pathway.
Source: Inflammatory Bowel Diseases - June 16, 2015 Category: Gastroenterology Tags: Original Basic Science Articles Source Type: research
The protective effect of piperine on dextran sulfate sodium induced inflammatory bowel disease and its relation with pregnane X receptor activation
Conclusion Piperine is a potential agonist of PXR and an inducer of PXR, which may induce CYP3A4 gene expression at the mRNA and protein levels. These results establish that piperine may contribute to prevention or reduction of colonic inflammation. Graphical abstract
Source: Journal of Ethnopharmacology - May 18, 2015 Category: Drugs & Pharmacology Source Type: research
Epithelial-specific ETS-1 (ESE1/ELF3) regulates apoptosis of intestinal epithelial cells in ulcerative colitis via accelerating NF-κB activation
In this study, we reported for the first time that ESE1/ELF3 was over-expressed in intestinal epithelial cells (IECs) of patients with UC. In DSS-induced colitis mouse models, we observed the up-regulation of ESE1/ELF3 accompanied with the elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and NF-κB activation indicators [phosphorylated NF-κB p65 subunit (p-p65) and p-IκB] in colitis IECs. Increased co-localization of ESE1/ELF3 with active caspase-3 (and p-p65) in IECs of the DSS-induced colitis group further indicated the possible involvement of ESE1/ELF3 in NF-κB-mediated IEC apoptosis in UC...
Source: Immunologic Research - April 30, 2015 Category: Allergy & Immunology Source Type: research
Effects of mannose density on in vitro and in vivo cellular uptake and RNAi efficiency of polymeric nanoparticles.
Abstract
To evaluate the effects of mannose density on in vitro and in vivo cellular uptake and RNA interference (RNAi) efficiency of polymeric nanoparticles (NPs) in macrophages, mannose-modified trimethyl chitosan-cysteine (MTC) conjugates with mannose densities of 4%, 13%, and 21% (MTC-4, MTC-13, and MTC-21) were synthesized. Tumor necrosis factor-alpha (TNF-α) siRNA loaded MTC NPs with particle sizes of ∼150 nm exhibited desired structural stability and effectively protected siRNA from enzymatic degradation. Generally, cellular uptake and RNAi efficiency were affected by mannose density. As expected, MTC...
Source: Biomaterials - April 1, 2015 Category: Materials Science Authors: Chu S, Tang C, Yin C Tags: Biomaterials Source Type: research
A Cell Type-Specific Role of Protein Tyrosine Phosphatase Non-Receptor Type 2 in Regulating ER Stress Signalling
Conclusions: Whereas the knockdown of PTPN2 made THP-1 cells more susceptible to ER stress, PTPN2 deficiency reduced ER stress responses in HT-29 IECs. This suggests that PTPN2 regulates adaptation to ER stress in a cell type-specific manner.Digestion 2015;91:248-256
Source: Digestion - March 25, 2015 Category: Gastroenterology Source Type: research
TNF-α inhibitor protects against myocardial ischemia/reperfusion injury via Notch1 mediated suppression of oxidative/nitrative stress.
This study aims to determine the involvement of TNF-a inhibitor with Notch1 in MI/R and delineate the related mechanism. Notch1 specific small interfering RNA (siRNA, 20μg) or Jagged1 (a Notch ligand, 12μg) was delivered through intramyocardial injection. 48h after injection, mice received 30min of myocardial ischemia followed by 3h (for cell apoptosis and oxidative/nitrative stress) and 24h (for infarct size and cardiac function) of reperfusion. 10min before reperfusion, mice randomly received intraperitoneal injection of vehicle, Etanercept, diphenyleneiodonium, 1400W or EUK134. Finally, downregulation of Notch1 signif...
Source: Free Radical Biology and Medicine - February 10, 2015 Category: Biology Authors: Pei H, Song X, Peng C, Tan Y, Li Y, Li X, Ma S, Wang Q, Huang R, Yang D, Li, Gao E, Yang Y Tags: Free Radic Biol Med Source Type: research
Citrus nobiletin ameliorates experimental colitis by reducing inflammation and restoring impaired intestinal barrier function
Conclusion: Nobiletin exerted anti‐inflammatory effects in TNBS‐induced colitis through the down‐regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX‐2) expression. Nobiletin restored barrier function, which had been damaged after TNBS administration, through the inhibition of the Akt–NF‐κB–MLCK pathway.This article is protected by copyright. All rights reserved
Source: Molecular Nutrition and Food Research - February 1, 2015 Category: Food Science Authors: Yongjian Xiong, Dapeng Chen, Changchun Yu, Bochao Lv, Jinyong Peng, Jingyu Wang, Yuan Lin Tags: Research Article Source Type: research
Vacuolar protein sorting 4B regulates apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease.
In this study, we reported for the first time that VPS4B was over-expressed in intestinal epithelial cell (IECs) of patients with CD. In TNBS-induced mouse colitis models, we observed the up-regulation of VPS4B was accompanied with the elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and phosphorylated p38 in colitis IECs. Co-localization of VPS4B and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of VPS4B in IEC apoptosis. Employing the TNF-α-treated HT29 cells as an in vitro IEC apoptosis model, we confirmed the positive correlation of VPS4B with caspase...
Source: Experimental and Molecular Pathology - December 20, 2014 Category: Pathology Authors: Zhang D, Wang L, Yan L, Miao X, Gong C, Xiao M, Ni R, Tang Q Tags: Exp Mol Pathol Source Type: research
PAR2 Reduces Colonic Epithelial Apoptosis Molecular Bases of Disease
Mucosal biopsies from inflamed colon of inflammatory bowel disease patients exhibit elevated epithelial apoptosis compared with those from healthy individuals, disrupting mucosal homeostasis and perpetuating disease. Therapies that decrease intestinal epithelial apoptosis may, therefore, ameliorate inflammatory bowel disease, but treatments that specifically target apoptotic pathways are lacking. Proteinase-activated receptor-2 (PAR2), a G protein-coupled receptor activated by trypsin-like serine proteinases, is expressed on intestinal epithelial cells and stimulates mitogenic pathways upon activation. We sought to determi...
Source: Journal of Biological Chemistry - December 4, 2014 Category: Chemistry Authors: Iablokov, V., Hirota, C. L., Peplowski, M. A., Ramachandran, R., Mihara, K., Hollenberg, M. D., MacNaughton, W. K. Tags: Cell Biology Source Type: research
Differential regulation of interleukin-8 and human beta-defensin 2 in Pseudomonas aeruginosa -infected intestinal epithelial cells
Conclusions:
The P. aeruginosa-induced antimicrobial peptide in IECs continuously protect the host against prolonged infection, while modulation of proinflammatory responses prevents the host from the detrimental effects of overwhelming inflammation. Thus, P. aeruginosa-induced innate immunity in IECs represents a host protective mechanism, which may provide new insight into the pathogenesis of inflammatory bowel diseases.
Source: BMC Microbiology - November 30, 2014 Category: Microbiology Authors: Fu-Chen Huang Source Type: research
Regulators of NOD2-induced IL-8 Secretion Signal Transduction
NOD2 encodes an intracellular multidomain pattern recognition receptor that is the strongest known genetic risk factor in the pathogenesis of Crohn disease (CD), a chronic relapsing inflammatory disorder of the intestinal tract. NOD2 functions as a sensor for bacterial cell wall components and activates proinflammatory and antimicrobial signaling pathways. Here, using a genome-wide small interfering RNA (siRNA) screen, we identify numerous genes that regulate secretion of the proinflammatory cytokine IL-8 in response to NOD2 activation. Moreover, many of the identified IL-8 regulators are linked by protein-protein interact...
Source: Journal of Biological Chemistry - October 9, 2014 Category: Chemistry Authors: Warner, N., Burberry, A., Pliakas, M., McDonald, C., Nunez, G. Tags: Immunology Source Type: research
Abstract 5358: IL-4/IL-13 induce Duox2/DuoxA2 expression and reactive oxygen production in human pancreatic and colon cancer cells
NADPH oxidase (NOX)-derived reactive oxygen species (ROS) contribute significantly to inflammation-associated carcinogenesis. Expression of dual oxidase 2 (Duox2), one of seven members of the NOX gene family, is up-regulated in inflammatory bowel disease, chronic pancreatitis, and in many human malignancies including carcinomas of the prostate, lung, and breast. Previously, we demonstrated that Stat1 and/or NF-κB play a critical role in modulating the enhanced expression of Duox2, and its cognate maturation factor DuoxA2, by IFN-γ and lipopolysaccharide in human pancreatic cancer cells. This cytokine-mediated increase in...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Wu, Y., Doroshow, J. H. Tags: Carcinogenesis Source Type: research
Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract
Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research
Disruption of macrophage pro-inflammatory cytokine release in Crohn's disease is associated with reduced optineurin expression in a subset of patients.
This article is protected by copyright. All rights reserved.
PMID: 24943399 [PubMed - as supplied by publisher]
Source: Immunology - June 18, 2014 Category: Allergy & Immunology Authors: Smith A, Sewell G, Levine A, Chew T, Dunne J, O'Shea N, Smith P, Harrison P, Macdonald C, Bloom S, Segal A Tags: Immunology Source Type: research
