| Autor: |
Naito Y; 1Department of Genomic Medicine,National Cerebral and Cardiovascular Center,Suita,Osaka 565-8565,Japan., Ji X; 1Department of Genomic Medicine,National Cerebral and Cardiovascular Center,Suita,Osaka 565-8565,Japan., Tachibana S; 4Hatano Research Institute,Food and Drug Safety Center,Hadano,Kanagawa 257-8523,Japan., Aoki S; 4Hatano Research Institute,Food and Drug Safety Center,Hadano,Kanagawa 257-8523,Japan., Furuya M; 4Hatano Research Institute,Food and Drug Safety Center,Hadano,Kanagawa 257-8523,Japan., Tazura Y; 4Hatano Research Institute,Food and Drug Safety Center,Hadano,Kanagawa 257-8523,Japan., Miyazawa D; 5College of Pharmacy,Kinjo Gakuin University,Nagoya,Aichi 463-8521,Japan., Harauma A; 6Department of Food and Life Science,School of Life and Environmental Science,Azabu University,Sagamihara,Kanagawa 252-0206,Japan., Moriguchi T; 6Department of Food and Life Science,School of Life and Environmental Science,Azabu University,Sagamihara,Kanagawa 252-0206,Japan., Nagata T; 4Hatano Research Institute,Food and Drug Safety Center,Hadano,Kanagawa 257-8523,Japan., Iwai N; 1Department of Genomic Medicine,National Cerebral and Cardiovascular Center,Suita,Osaka 565-8565,Japan., Ohara N; 5College of Pharmacy,Kinjo Gakuin University,Nagoya,Aichi 463-8521,Japan. |
| Abstrakt: |
The aim of this study was to investigate the effects of the administration of oral arachidonic acid (AA) in rats with or without dextran sulphate sodium (DSS)-induced inflammatory bowel disease. Male Wistar rats were administered AA at 0, 5, 35 or 240 mg/kg daily by gavage for 8 weeks. Inflammatory bowel disease was induced by replacing drinking water with 3 % DSS solution during the last 7 d of the AA dosing period. These animals passed loose stools, diarrhoea and red-stained faeces. Cyclo-oxygenase-2 concentration and myeloperoxidase activity in the colonic tissue were significantly increased in the animals given AA at 240 mg/kg compared with the animals given AA at 0 mg/kg. Thromboxane B2 concentration in the medium of cultured colonic mucosae isolated from these groups was found to be dose-dependently increased by AA, and the increase was significant at 35 and 240 mg/kg. Leukotriene B4 concentration was also significantly increased and saturated at 5 mg/kg. In addition, AA at 240 mg/kg promoted DSS-induced colonic mucosal oedema with macrophage infiltration. In contrast, administration of AA for 8 weeks, even at 240 mg/kg, showed no effects on the normal rats. These results suggest that in rats with bowel disease AA metabolism is affected by oral AA, even at 5 mg/kg per d, and that excessive AA may aggravate inflammation, whereas AA shows no effects in rats without inflammatory bowel disease. |
