Emu Oil Increases Colonic Crypt Depth in a Rat Model of Ulcerative Colitis

2011 ◽  
Vol 57 (4) ◽  
pp. 887-896 ◽  
Author(s):  
Suzanne M. Abimosleh ◽  
Ruth J. Lindsay ◽  
Ross N. Butler ◽  
Adrian G. Cummins ◽  
Gordon S. Howarth
2020 ◽  
Vol 245 (18) ◽  
pp. 1697-1707
Author(s):  
Chloe J Mitchell ◽  
Gordon S Howarth ◽  
Lauren C Chartier ◽  
Debbie Trinder ◽  
Ian C Lawrance ◽  
...  

Crohn’s disease is a severe, incurable inflammatory bowel disease. Orally administered emu oil has demonstrated anti-inflammatory properties in previous models of gastrointestinal disease. We aimed to determine whether orally administered emu oil could attenuate disease in a mouse model of Crohn’s-like colitis. Female ARC(s) mice (CD-1 equivalent, n = 10/group) were intra-rectally administered water (120 μL) or trinitrobenzene sulfonic acid (TNBS; 3 mg in 50% ethanol; 120 μL bolus) on day 0. Mice were orally administered water (80 μL) or emu oil (80 μL or 160 μL) daily for five days and euthanized on day six. Bodyweight and disease activity were recorded daily. Colonoscopy, burrowing activity, facial grimace, histological parameters (damage severity, small intestinal villus height/crypt depth and colonic crypt depth), myeloperoxidase activity and intestinal permeability were assessed. P < 0.05 was considered statistically significant. TNBS decreased bodyweight (days 1, 2, 4; P < 0.05) and increased disease activity (days 1–6; P < 0.01), compared to normal controls. Emu oil (80 μL) attenuated disease activity on days 5–6 ( P < 0.05), although bodyweight loss was not significantly impacted ( P > 0.05). Facial grimace and colonoscopy scores were significantly increased in TNBS-control mice; effects attenuated by both volumes of emu oil ( P < 0.001). TNBS increased histological damage severity compared to normal controls ( P < 0.05); an effect attenuated by 80 μL emu oil (proximal and distal colon; P < 0.05) and 160 μL emu oil (distal colon; P < 0.01). In the ileum, villus height and crypt depth were unaffected by TNBS or emu oil treatment compared to normal ( P > 0.05). TNBS-induced distal colonic crypt lengthening was unaffected following emu oil administration ( P > 0.05). Remaining parameters, including burrowing, myeloperoxidase activity and intestinal permeability, were unchanged across all treatment groups ( P > 0.05). In normal mice, emu oil treatment did not significantly impact any parameter compared to normal controls. In conclusion, emu oil reduced overall disease severity and facial grimace scores in TNBS mice. These results suggest therapeutic potential for orally administered emu oil in the management of Crohn’s disease.


2015 ◽  
Vol 76 (4) ◽  
pp. 204-214 ◽  
Author(s):  
Amal J. Fatani ◽  
Khaled A. Al-Hosaini ◽  
Mohammed M. Ahmed ◽  
Hatem M. Abuohashish ◽  
Mihir Y. Parmar ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Yuan Liu ◽  
Xin-Yue Wang ◽  
Xue Yang ◽  
Shan Jing ◽  
Li Zhu ◽  
...  

Background. To investigate the link and mechanisms between intestine and lung in the ulcerative colitis (UC) rat model.Materials and Methods. We used the UC rat model by immunological sensitization combined with local 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) in 50% ethanol enema, observed dynamically animal general state and body weight, examined the histological and functional changes in the colon, lung, liver, and kidney tissues, and detected microvascular endothelium response towards inflammation characterized with the expression of iNOS, TXB2, P-selectin, ICAM-1, and vascular endothelial growth factor A (VEGF-A) in the colon and lung tissue.Results. Pulmonary function results suggested ventilator disorder, and pathological findings showed interstitial pneumonia. There were no significant changes in the liver and kidney function and histopathology. The colon and lung tissue iNOS, TXB2, P-selectin, ICAM-1, and VEGF-A expression of the model rats was significantly higher than the normal rats at both time points.Conclusions. Our study is the first to demonstrate the close association between the large intestine and lung in the immune-TNBS-ethanol-induced UC rat model. Different organs and tissues with the same embryonic origin may share the same pathological specificities in a disease. The present study provided a new way of thinking for pathological changes in clinical complex diseases manifested with multiorgan damage.


2009 ◽  
Vol 136 (5) ◽  
pp. A-717
Author(s):  
Ruth J. Lindsay ◽  
Mark S. Geier ◽  
Roger Yazbeck ◽  
Kerry A. Lymn ◽  
Ross N. Butler ◽  
...  
Keyword(s):  

2007 ◽  
Vol 292 (3) ◽  
pp. R1081-R1091 ◽  
Author(s):  
Junqiang Tian ◽  
Naohiro Washizawa ◽  
Li H. Gu ◽  
Marc S. Levin ◽  
Lihua Wang ◽  
...  

Limited data in animal models suggest that colonic mucosa undergoes adaptive growth following massive small bowel resection (SBR). In vitro data suggest that intestinal cell growth is regulated by reactive oxygen species and redox couples [e.g., glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) redox]. We investigated the effects of SBR and alterations in redox on colonic growth indexes in rats after either small bowel transection (TX) or 80% midjejunoileal resection (RX). Rats were pair fed ± blockade of endogenous GSH synthesis with buthionine sulfoximine (BSO). Indexes of colonic growth, proliferation, and apoptosis and GSH/GSSG and Cys/CySS redox potentials (Eh) were determined. RX significantly increased colonic crypt depth, number of cells per crypt, and epithelial cell proliferation [crypt cell bromodeoxyuridine (BrdU) incorporation]. Administration of BSO markedly decreased colonic mucosal GSH, GSSG, and Cys concentrations in both TX and RX groups, with a resultant oxidation of GSH/GSSG and Cys/CySS Eh. BSO did not alter colonic crypt cell apoptosis but significantly increased all colonic mucosal growth indexes (crypt depth, cells/crypt, and BrdU incorporation) in both TX and RX groups in a time- and dose-dependent manner. BSO significantly decreased plasma GSH and GSSG, oxidized GSH/GSSG Eh, and increased plasma Cys and CySS concentrations. Collectively, these data provide in vivo evidence indicating that oxidized colonic mucosal redox status stimulates colonic mucosal growth in rats. The data also suggest that GSH is required to maintain normal colonic and plasma Cys/CySS homeostasis in these animal models.


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