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Sulphasalazine and experimental stress ulcers.

C W Ogle, C H Cho, S Dai

    Agents and Actions
    |December 1, 1985
    PubMed
    Summary

    Sulphasalazine protects against stress-induced gastric ulcers in rats, independent of prostaglandin E2 (PGE2) levels. Its protective mechanism may involve inhibiting lipoxygenase activity, offering a new therapeutic avenue.

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    The Co-regulatory Role of 5-Lipoxygenase and Cyclooxygenase-2 in the Carcinogenesis and their Promotion by Cigarette Smoking in Colons.

    Current medicinal chemistry·2016

    Area of Science:

    • Gastroenterology
    • Pharmacology

    Background:

    • Stress-induced gastric ulceration is a significant clinical concern.
    • Prostaglandin E2 (PGE2) is implicated in gastric mucosal protection.
    • Sulphasalazine is a drug with anti-inflammatory properties.

    Purpose of the Study:

    • To investigate the effects of sulphasalazine on stress-induced gastric ulceration in rats.
    • To determine the role of prostaglandin E2 (PGE2) in sulphasalazine's antiulcer activity.
    • To explore the potential mechanism of sulphasalazine's protective effects.

    Main Methods:

    • Gastric ulceration was induced in rats by restraint stress at 4°C.
    • Sulphasalazine was administered subcutaneously at doses of 63 or 125 mg/kg.
    • Gastric mucosal PGE2 levels were measured using established assays.
    • Lesion formation was assessed macroscopically.
    • The effects of indomethacin and exogenous PGE2 were also evaluated.

    Main Results:

    • Sulphasalazine (63 or 125 mg/kg) prevented stress-induced gastric ulceration without altering PGE2 levels.
    • Indomethacin pretreatment worsened stress ulceration and reduced PGE2 levels.
    • Exogenous PGE2 administration did not protect against stress ulceration.
    • Sulphasalazine did not counteract the ulcerogenic effects of indomethacin combined with stress.

    Conclusions:

    • Sulphasalazine's antiulcer activity in stress-induced gastric ulceration is not mediated by changes in gastric PGE2 levels.
    • The protective mechanism of sulphasalazine may involve the inhibition of lipoxygenase activity.
    • These findings suggest a novel therapeutic potential for sulphasalazine in managing stress-related gastrointestinal issues.

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