scholarly journals Dextran Sodium Sulfate-induced Colitis as a Model for Sarcopenia in Mice

2019 ◽  
Vol 26 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Dominik Saul ◽  
Robyn Laura Kosinsky

Forty-two percent of inflammatory bowel disease patients suffer from sarcopenia. We established a mouse model for this condition. Dextran sodium sulfate–induced colitis caused a severe decrease in muscle mass, fiber size, and the regulation of sarcopenia-associated key players on mRNA level.

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Thomas Köhnke ◽  
Beate Gomolka ◽  
Süleyman Bilal ◽  
Xiangzhi Zhou ◽  
Yanping Sun ◽  
...  

The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used to assess disease severity, and lipid metabolites were measured using liquid chromatography-coupled tandem mass spectrometry. Decreased colitis activity was demonstrated by phenotype and MRI assessment in mice treated with ASA, and confirmed in postmortem analysis. Analysis of lipid mediators showed sustained formation of lipoxin A4 and an increase of DHA-derived 17-hydroxydocosahexaenoic acid (17-HDHA) after treatment with ASA. Furthermore,in vitroexperiments in RAW264.7 murine macrophages demonstrated significantly increased phagocytosis activity after incubation with 17-HDHA, supporting its proresolution effect. These results show a protective effect of ASA in a murine colitis model and could give a rationale for a careful reassessment of ASA therapy in patients with inflammatory bowel disease and particularly ulcerative colitis, possibly combined with DHA supplementation.


2019 ◽  
Vol 22 (7) ◽  
pp. 672-679 ◽  
Author(s):  
Jin-Sil Park ◽  
JeongWon Choi ◽  
Sun-Hee Hwang ◽  
Jae-Kyung Kim ◽  
Eun-Kyung Kim ◽  
...  

2008 ◽  
Vol 134 (4) ◽  
pp. A-260
Author(s):  
Gary C. Bruns ◽  
Dave Cody ◽  
Russell J. Sheldon ◽  
George Zhang

2015 ◽  
Vol 10 (4) ◽  
pp. 860
Author(s):  
Irfan Ahmad Rather ◽  
Vivek K. Bajpai ◽  
Nam Gyeong-Jun

<p>Animal model of intestinal inflammation is of paramount significance that aids in discerning the pathologies underlying ulcerative colitis and Crohn’s disease, the two clinical presentations of inflammatory bowel disease. The 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis model represents one such intestinal inflammation-prototype that is generated in susceptible strains of mice through intra-rectal instillation of compound TNBS. In this paper, we demonstrate the experimental induction of TNBS-mediated colitis in a susceptible strain of ICR mice. This can be done by the following steps: a) acclimation, b) induction and c) observation. TNBS-mouse model provides the information in shortest possible time and simultaneously represents a cost effective and highly reproducible model method of studying the pathogenesis of inflammatory bowel disease.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/6MsuIGzH3uA">Acclimation and induction of TNBS</a>:          4.5 min</p><p><a href="https://youtube.com/v/ya66SNwoVag">Observation and drug administration</a>:      1.5 min</p>


2015 ◽  
Vol 21 (1) ◽  
pp. 051-061 ◽  
Author(s):  
Jae Hyung Park ◽  
Joong Goo Kwon ◽  
Sun Joo Kim ◽  
Dae Kyu Song ◽  
Seok Guen Lee ◽  
...  

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