Fertility and sterility · 2007
Effects of progesterone on FSH-stimulated indomethacin ulcers in rats.
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Borekci Bunyamin, Cadirci Elif, Albayrak Abdulmecit, Suleyman Halis, Halici Zekai, Kadanali Sedat
Аннотация
OBJECTIVE: To investigate whether the balance between progesterone and FSH levels has a role in ulcer formation/inhibition.
DESIGN: Animal study.
SETTING: Ataturk University, Faculty of Medicine, Laboratory of Pharmacology Department.
PATIENT(S): One hundred thirty-two female Albino Wistar rats.
INTERVENTION(S): Ovariectomy. Chronic administration of progesterone and estrogen to ovariectomized rats. Acute administration of progesterone to ovariectomized rats. Acute administration of progesterone and FSH to intact rats. Combined administration of mifepristone with progesterone or FSH to intact rats. Indomethacin administration to all rats.
MAIN OUTCOME MEASURE(S): Gastric ulcer areas as mm(2).
RESULT(S): Indomethacin-induced ulcers were significantly higher in ovariectomized rats than in intact rats. Chronic progesterone (1 mg/kg) inhibited gastrointestinal system ulcers by 51.2%, whereas 2 and 5 mg/kg chronic progesterone and 1, 2, and 5 mg/kg chronic estrogen were not effective. Acute progesterone (5 mg/kg) increased indomethacin ulcers significantly in ovariectomized rats. FSH increased indomethacin ulcers significantly. In addition, progesterone increased indomethacin ulcers significantly in intact rats. Mifepristone antagonized the ulcerogenic effects of FSH and progesterone.
CONCLUSION(S): Our data suggest that progesterone is not an antiulcer hormone, and produces ulcers via its own receptor. In addition, FSH may produce ulcerogenic effects via progesterone receptors. The low doses of progesterone (inhibits endogenous FSH) cannot stimulate its own receptors sufficiently for ulcer formation and prevent the ulcerogenic effects of FSH by decreasing FSH concentration.
DESIGN: Animal study.
SETTING: Ataturk University, Faculty of Medicine, Laboratory of Pharmacology Department.
PATIENT(S): One hundred thirty-two female Albino Wistar rats.
INTERVENTION(S): Ovariectomy. Chronic administration of progesterone and estrogen to ovariectomized rats. Acute administration of progesterone to ovariectomized rats. Acute administration of progesterone and FSH to intact rats. Combined administration of mifepristone with progesterone or FSH to intact rats. Indomethacin administration to all rats.
MAIN OUTCOME MEASURE(S): Gastric ulcer areas as mm(2).
RESULT(S): Indomethacin-induced ulcers were significantly higher in ovariectomized rats than in intact rats. Chronic progesterone (1 mg/kg) inhibited gastrointestinal system ulcers by 51.2%, whereas 2 and 5 mg/kg chronic progesterone and 1, 2, and 5 mg/kg chronic estrogen were not effective. Acute progesterone (5 mg/kg) increased indomethacin ulcers significantly in ovariectomized rats. FSH increased indomethacin ulcers significantly. In addition, progesterone increased indomethacin ulcers significantly in intact rats. Mifepristone antagonized the ulcerogenic effects of FSH and progesterone.
CONCLUSION(S): Our data suggest that progesterone is not an antiulcer hormone, and produces ulcers via its own receptor. In addition, FSH may produce ulcerogenic effects via progesterone receptors. The low doses of progesterone (inhibits endogenous FSH) cannot stimulate its own receptors sufficiently for ulcer formation and prevent the ulcerogenic effects of FSH by decreasing FSH concentration.