Dietary polyunsaturated fatty acids improve histological and biochemical alterations in rats with experimental ulcerative colitis.
The aim of the present study was to determine whether dietary intake of monounsaturated (MUFA) and/or polyunsaturated fatty acids (PUFA) of the (n- 3) and (n-6) series could improve intestinal damage and reduce inflammation in experimental ulcerative colitis (UC). Rats were treated with 80 mg/kg body of 2,4,6-trinitrobenzenesulfonic acid and fed for 1 or 2 wk diets enriched in olive oil (OO), fish oil (FO), or purified pig brain phospholipids (BPL), as sources of monounsaturated and PUFA of the (n-3) and (n-3) + (n-6) series. Evaluation of macroscopic and microscopic colonic damage was assessed. Ultrastructural and histologic changes were analyzed as well as plasma and colonic mucosa fatty acid profiles and some biochemical markers of injury and inflammation [alkaline phosphatase (AP), mieloperoxidase (MPO), prostaglandin E(2) (PGE(2)) and leukotriene B(4)]. Fatty acid profiles of both plasma and mucosa mostly reflected the dietary fatty acid composition. Plasma MUFA proportions were higher in UC animals fed the OO diet compared with FO or BPL groups 1 and 2 wk and (n-3) long chain PUFA (LC-PUFA) were higher in the FO than in the OO and BPL groups. At 1 wk, UC led to lower MUFA mucosa levels and (n-3)LC-PUFA were higher in the FO group compared with the OO and BPL groups. Rats with UC fed FO at 1 wk showed significantly less macroscopic and microscopic colonic damage. They also have lower AP and MPO activities and PGE(2) levels compared with the OO and BPL groups and showed enhanced histological repair, less necrotic areas within the mucosa, and more goblet cells with mature mucin granules. These results suggest that the use of balanced diets containing (n-3) LC-PUFA could ameliorate the inflammation and mucosal damage in UC.
Nieto
Natalia
N
Department of Biochemistry and Molecular Biology, University of Granada, 18071 Granada, Spain.
Torres
María Isabel
MI
Ríos
Antonio
A
Gil
Angel
A
D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure; D015232:Dinoprostone / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage / Q000378:metabolism; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage* / Q000097:blood / Q000378:metabolism*; D005395:Fish Oils; D007413:Intestinal Mucosa / Q000166:cytology / Q000473:pathology* / Q000648:ultrastructure; D007975:Leukotriene B4 / Q000378:metabolism; D008297:Male; D000069463:Olive Oil; D010938:Plant Oils; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid
D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated; D005395:Fish Oils; D000069463:Olive Oil; D010938:Plant Oils; D007975:Leukotriene B4; D014302:Trinitrobenzenesulfonic Acid; D000469:Alkaline Phosphatase; D015232:Dinoprostone