Prebiotics Fructo-, Galacto-, and Mannan-Oligosaccharide Do Not Protect against 5-Fluorouracil-Induced Intestinal Mucositis in Rats.

BACKGROUND: Prebiotics selectively stimulate the growth of beneficial bacteria within the gastrointestinal tract, and have been investigated in human and animal studies for their capacity to improve intestinal health. OBJECTIVE: We investigated the prebiotics fructo-oligosaccharide (FOS), galacto-oligosaccharide (GOS), and mannan-oligosaccharide (MOS) for their potential to alleviate intestinal damage in rats. METHODS: Female Dark Agouti rats (6-8 wk old, 110-150 g) were allocated to 1 of the following treatment groups (n = 8/group): saline/water, saline/FOS, saline/GOS, saline/MOS, 5-fluorouracil (5FU)/water, 5FU/FOS, 5FU/GOS, and 5FU/MOS. Rats were pretreated with either 5% GOS, MOS, or FOS or vehicle (water) from day -12 to day 0. On day 0, rats received a single intraperitoneal injection of saline or 5FU. Metabolic data were recorded daily and all rats were killed on day 3. Histopathology was quantified in hematoxylin and eosin-stained sections. Intestinal sucrase and myeloperoxidase activity were quantified by biochemical assay. Fecal SCFAs-acetic, propionic, and butyric acid-were also measured. Statistical analysis was by repeated-measures, 2-factor ANOVA or Kruskal-Wallis and Mann-Whitney U test; P < 0.05 was considered statistically significant. RESULTS: Body weight was significantly decreased in all treatment groups after 5FU injection, with no change in body weight observed in any prebiotic treatment group. Total food intake was lower by ≥7% in the GOS treatment group pre-5FU than in all other groups (P < 0.05). Ileal villus height was 18% higher in GOS-treated rats pre-5FU than in respective water controls (P < 0.05). Jejunal and ileal villus height and crypt depth were significantly decreased in all treatment groups after 5FU injection, with no prebiotic effect observed. SCFAs were differentially increased in prebiotic treatment groups compared with water-only controls (P < 0.05). CONCLUSIONS: FOS, GOS, and MOS have differential effects in modifying small intestinal pathology and SCFA profiles in rats with healthy and damaged small intestinal mucosa.

Emu oil increases colonic crypt depth in a rat model of ulcerative colitis.

BACKGROUND: Current treatments for the inflammatory bowel diseases, encompassing Crohn's disease and ulcerative colitis, are variably effective. Emu oil, extracted from emu fat, predominantly comprises fatty acids, with purported claims of anti-inflammatory properties. AIM: We evaluated emu oil for its potential to ameliorate dextran sulphate sodium (DSS)-induced colitis in rats. METHODS: Male Sprague-Dawley Rats were allocated to treatment groups (n = 8). Groups 1 and 2 consumed water and were gavaged (1 ml) daily with water (group 1) or emu oil (group 2) from days 0 to 10. Groups 3-6 ingested 2% DSS in the drinking water from days 5 to 10 and were gavaged from days 0 to 10 with water (group 3), 0.5 ml emu oil (group 4) or 1 ml emu oil (group 5). Group 6 received 1 ml emu oil after commencing DSS treatment (days 6-10). Disease activity index, metabolic parameters, (13)C-sucrose breath test, and histological colonic damage severity and crypt depth were assessed. RESULTS: Emu oil in DSS-treated rats reduced colonic damage severity compared to DSS-controls (up to threefold; P < 0.001). In DSS-treated rats, crypts in the proximal colon were lengthened by 0.5 ml emu oil (373 ± 18 µm), compared with DSS-controls (302 ± 8 µm); whilst in the distal colon (DSS control: 271 ± 17 µm), crypt depth was greater following 0.5 ml emu oil (352 ± 22 µm) and 1 ml emu oil (341 ± 9 µm) and also when emu oil was administered post-DSS commencement (Group 6: 409 ± 16 µm; P < 0.05). Emu oil did not significantly affect other parameters of colonic architecture. CONCLUSIONS: Emu oil improved tissue damage associated with colitis, suggesting its potential as a unique formulation to augment conventional treatment approaches for IBD.

Orally administered emu oil decreases acute inflammation and alters selected small intestinal parameters in a rat model of mucositis.

Mucositis resulting from cancer chemotherapy is a serious disorder of the alimentary tract. Emu oil has demonstrated anti-inflammatory properties in animal models of arthritis and wound healing; however, its effects on the intestine remain unknown. We investigated emu oil for its potential to decrease the severity of mucositis in a rat model. Female Dark Agouti rats (110-150 g) were orogastrically gavaged with emu oil (0.5 or 1 ml) or water (1 ml) for 5 d before intraperitoneal injection of 5-fluorouracil (5-FU, 150 mg/kg) or saline (control), and this was continued up to the day of sacrifice (48, 72 and 96 h post 5-FU administration). Histological (villus height, crypt depth (CD) and disease severity score) and biochemical (myeloperoxidase (MPO) activity) parameters were determined in intestinal tissues collected at sacrifice. Sucrase activity in vivo was quantified by the sucrose breath test. Activated neutrophil activity (MPO) in the ileum was significantly decreased by emu oil (0.5 ml, 451 (sem 168) U/g and 1 ml, 503 (sem 213) U/g) compared with 5-FU-treated controls (1724 (sem 431) U/g) 96 h post 5-FU administration. There were also significant increases in CD (152 (sem 8) microm) in the ileum of rats that received 1 ml emu oil at 96 h compared with 5-FU-treated controls (CD (106 (sem 12) microm)). Emu oil did not affect sucrase activity. Emu oil decreased acute ileal inflammation, and improved mucosal architecture in the intestine during recovery from chemotherapy in rats. Further studies investigating the potential benefits of emu oil as a nutritional supplement for the treatment of intestinal disorders are indicated.