OBJECTIVE: To evaluate anti-ulcer effect of estrogen and luteinising hormone (LH) on indomethacin-induced ulcer model in female rats. STUDY DESIGN: Ovariectomy in healthy adult famale rats. Acute administration of estradiol to ovariectomised rats. Acute administration of LH to intact rats. Combined administration of tamoxifen with estradiol or LH to intact rats. Combined administration of yohimbin with estradiol or LH to intact rats. Combined administration of piperoxan with estradiol or LH to intact rats. Indomethacin administration to all rats. RESULTS: Results have shown that LH exerted anti-ulcer activity at all doses we used but estradiol at 5 and 10 mg/kg. In rats administered yohimbine and piperoxan estradiol and LH could not prevent indomethacin-induced ulcers. In rats administered tamoxifen, estradiol and LH could prevent indomethacin-induced ulcers. CONCLUSIONS: LH is a very potent endogen anti-ulcer factor, and the anti-ulcerative activities of estrogen and LH are mediated via alpha-2 adrenergic receptors, but not es receptors. The resistance of gastric mucosa to aggressive factors may decrease as a result of LH inhibition when estrogen is secreted chronically in the human body.
OBJECTIVE: To evaluate anti-ulcer effect of estrogen and luteinising hormone (LH) on indomethacin-induced ulcer model in female rats. STUDY DESIGN: Ovariectomy in healthy adult famale rats. Acute administration of estradiol to ovariectomised rats. Acute administration of LH to intact rats. Combined administration of tamoxifen with estradiol or LH to intact rats. Combined administration of yohimbin with estradiol or LH to intact rats. Combined administration of piperoxan with estradiol or LH to intact rats. Indomethacin administration to all rats. RESULTS: Results have shown that LH exerted anti-ulcer activity at all doses we used but estradiol at 5 and 10 mg/kg. In rats administered yohimbine and piperoxan estradiol and LH could not prevent indomethacin-induced ulcers. In rats administered tamoxifen, estradiol and LH could prevent indomethacin-induced ulcers. CONCLUSIONS:LH is a very potent endogen anti-ulcer factor, and the anti-ulcerative activities of estrogen and LH are mediated via alpha-2 adrenergic receptors, but not es receptors. The resistance of gastric mucosa to aggressive factors may decrease as a result of LH inhibition when estrogen is secreted chronically in the human body.