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A total of eighteen piglets (25\u00a0d old) were randomly allocated to one of three treatment groups (control, ACA and TBU). The control and ACA groups were fed a basal diet and the TBU group was fed the basal diet supplemented with 0\u00b71\u00a0% TBU. On day 15 of the trial, under anaesthesia, a soft catheter was inserted into the rectum of piglets (20\u201325\u00a0cm from the anus), followed by administration of either saline (control group) or ACA (10\u00a0ml of 10\u00a0% ACA solution for ACA and TBU groups). On day 22 of the trial, after venous blood samples were collected, piglets were killed to obtain mid-ileum and mid-colon mucosae. Compared with the control group, the ACA group exhibited an increase (<jats:italic>P<\/jats:italic>&lt;\u00a00\u00b705) in lymphocyte counts, creatinine, PGE<jats:sub>2<\/jats:sub>, and malondialdehyde concentrations and diamine oxidase and inducible NO synthase activities in the plasma and lymphocyte density in the colon and a decrease in insulin concentrations and glutathione peroxidase activity, ileal villus height:crypt depth ratios and goblet cell numbers in the colon. These adverse effects of ACA were attenuated by TBU supplementation. Moreover, TBU prevented the ACA-induced increase in caspase-3 levels while enhancing claudin-1 protein and epidermal growth factor receptor (<jats:italic>EGFR<\/jats:italic>) mRNA expression in the colonic mucosa. Collectively, these results indicate that dietary supplementation with 0\u00b71\u00a0% TBU alleviates ACA-induced intestinal injury possibly by inhibiting apoptosis, promoting tight-junction formation and activating EGFR signalling.<\/jats:p>","DOI":"10.1017\/s0007114514000038","type":"journal-article","created":{"date-parts":[[2014,2,10]],"date-time":"2014-02-10T08:48:26Z","timestamp":1392022106000},"page":"1748-1758","source":"Crossref","is-referenced-by-count":72,"title":["Dietary supplementation with tributyrin alleviates intestinal injury in piglets challenged with intrarectal administration of acetic 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