Hindawi Publishing Corporation Evidence-Based Complementary and Alternative Medicine Volume 2013, Article ID 429706, 10 pages http://dx.doi.org/10.1155/2013/429706 Research Article Emu Oil Reduces Small Intestinal Inflammation in the Absence of Clinical Improvement in a Rat Model of Indomethacin-Induced Enteropathy Suzanne M. Abimosleh, 1,2 Cuong D. Tran, 1,2 and Gordon S. Howarth 1,2,3 1 Department of Gastroenterology, Women’s and Children’s Hospital, North Adelaide, SA 5006, Australia 2 Discipline of Physiology, School of Medical Sciences, Faculty of Health Sciences, he University of Adelaide, Adelaide, SA 5005, Australia 3 School of Animal and Veterinary Sciences, he University of Adelaide, Roseworthy Campus, Roseworthy, SA 5371, Australia Correspondence should be addressed to Gordon S. Howarth; gordon.howarth@adelaide.edu.au Received 28 November 2012; Revised 4 February 2013; Accepted 13 February 2013 Academic Editor: Rocio De la Puerta Copyright © 2013 Suzanne M. Abimosleh et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Nonsteroidal-anti-inlammatory-drug (NSAID) enteropathy is characterized by small intestinal damage and ulceration. Emu Oil (EO) has previously been reported to reduce intestinal inlammation. Aim. We investigated EO for its potential to attenuate NSAID- enteropathy in rats. Methods. Male Sprague Dawley rats ( = 10/group) were gavaged with Water, Olive Oil (OO), or EO (0.5 mL; days 0–12) and with 0.5mL Water or the NSAID, Indomethacin (8mg/kg; days 5–12) daily. Disease activity index (DAI), 13C- sucrose breath test (SBT), organ weights, intestinal damage severity (IDS), and myeloperoxidase (MPO) activity were assessed.  < 0.05 was considered signiicant. Results. In Indomethacin-treated rats, DAI was elevated (days 10–12) and SBT values (56%) and thymus weight (55%) were decreased, relative to normal controls. Indomethacin increased duodenum (68%), colon (24%), SI (48%), caecum (48%), liver (51%) and spleen (88%) weights, IDS scores, and MPO levels (jejunum: 195%, ileum: 104%) compared to normal controls. Jejunal MPO levels were decreased (64%) by both EO and OO, although only EO decreased ileal MPO (50%), compared to Indomethacin controls. Conclusions. EO reduced acute intestinal inlammation, whereas other parameters of Indomethacin- induced intestinal injury were not afected signiicantly. Increased EO dose and/or frequency of administration could potentially improve clinical eicacy. 1. Introduction Nonsteroidal anti-inlammatory drugs (NSAIDs) are among the most widely prescribed pharmaceutical agents, with approximately 30 million patients worldwide ingesting NSAIDs daily [1, 2]. NSAIDs have been indicated as an efective treatment option for rheumatic and musculoskeletal conditions [3] and to potentially lower the risk of cardio- vascular and cerebrovascular insults. Indeed, recent studies have indicated eicacy for the treatment of colon cancer [2, 4]. NSAIDs represent a highly efective class of drug; however, their use is oten associated with a broad spectrum of adverse efects, predominantly within the gastrointesti- nal (GI) tract [2, 3]. he adverse events in the stomach, duodenum, jejunum, and ileum are collectively termed NSAID-gastroenteropathy [5]. NSAID-associated intestinal toxicity has several manifes- tations including increased mucosal permeability, inlamma- tion and ulceration, and in severe cases, bowel perforation [5]. Clinically evident features include anaemia, bleeding, mucosal diaphragms, strictures, and chronic bowel inlam- mation [6]. Serious injury to the small intestine (SI) has been estimated to account for one-third of all NSAID-associated complications [6]. he pathogenesis of NSAID-enteropathy is proposed to commence via a direct intestinal insult together with its enterohepatic and consequent systemic efects [3, 5, 7]. Entrance of the acidic NSAID into enterocytes induces