Study on the experimental ulcerative colitis(UC) model induced by dextran sulfate sodium(DSS) in rats. (3).

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  • KIMURA Isami
    Preclinical Development Laboratories, Nippon Hoechst Marion Roussel Ltd.
  • NAGAHAMA Shinobu
    Preclinical Development Laboratories, Nippon Hoechst Marion Roussel Ltd.
  • KAWASAKI Maki
    Preclinical Development Laboratories, Nippon Hoechst Marion Roussel Ltd.
  • KATAOKA Mikiko
    Preclinical Development Laboratories, Nippon Hoechst Marion Roussel Ltd.
  • SATO Makoto
    Preclinical Development Laboratories, Nippon Hoechst Marion Roussel Ltd.

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  • ラットにおけるデキストラン硫酸誘発潰よう性大腸炎モデルに関する基礎的研究　（第３報）　各種阻害剤の直腸内投与による影響
  • ラット ニ オケル デキストラン リュウサン ユウハツ カイヨウセイ ダイチョ

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Abstract

We have already confirmed that symptoms in the experimental UC model in rats induced by ingesting DSS resembled those of human UC. In the present study, to clarify the participation of chemical mediators concerned with the development and etiology of the experimental UC model, we investigated the effects of superoxide dismutase (SOD), 5-aminosalicylic acid (5-ASA), AA-861, an LTB4-receptor antagonist (LTB4-ra), indomethacin (Ind) and OKY-046 on the DSS-induced UC model in rats. The UC model was produced by giving rats drinking water containing 3% DSS, and animals were selected when bloody stool was observed in more than 90% of the animals. After selection, drugs were intrarectally administered once a day, for 7 days, to UC rats that were given drinking water containing 1 % DSS. SOD, 5-ASA, AA-861 and LTB4-ra inhibited the formation of erosions in the large intestine. Furthermore, SOD, 5-ASA and LTB4-ra improved the length of the large intestine of rats that had been shortened by ingesting DSS. On the other hand, neither Ind nor OKY-046 improved the shortening and erosion of the large intestine. From these results, it is concluded that the free radical and lipoxygenase metabolites of arachidonic acid may be partially involved in the DSS-induced UC model in rats.

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