Effect of Estrogen on Basal, Charbacol Stimulated Acid Secretion and Indomethacin Induced Ulcer in Female Albino Rats
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- Category: Vol. 80, September 2012
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Effect of Estrogen on Basal, Charbacol Stimulated Acid Secretion and Indomethacin Induced Ulcer in Female Albino Rats, NASHWA M.S. EL-TABLAWY, MOHAMED M. OMRAN, AKEF A. KHOWAILED and EMAD EL-DIN M.A. TANTAWY
Abstract
Introduction: Peptic ulcer occurs more frequently in men than in women, sex differences are less marked after 45 years of age probably because the incidence of ulcer increases in post menopausal women. The general assumption is that the ulcer differences between sexes are related in some way to sex hormones and that the female sex hormones protect against ulceration.
The aim of the this study was to investigate in rats the effect of ovariectomy on gastric acid secretion and gastric ulcer and to demonstrate the effect of estrogen, a selective alpha estrogen receptor agonist 1, 3, 5-tris (4-hydroxyphenyl)- 4-propyl-1H-pyrazol (PPT) and a selective beta estrogen receptor agonist 2, 3-bis (4-Hydroxyphenyl) Propionitrile (DPN) on gastric acid secretion on basal, charbacol stimulated acid secretion and also its effect on indomethacin induced ulcer in ovariectomized rats.
Material and Methods: A total of 90 female albino rats weighing 150-200gm were included in the study. The animals were divided into five groups 18 rats each.
•Group I: The control group.
•Group II: Was subjected to ovariectomy.
•Group III: Was subjected to ovariectomy and estrogen replacement therapy at a dose of 10μg/rat/day for ten days.
•Group IV: Was subjected to ovariectomy and a selective alpha estrogen receptor agonist 1, 3, 5-tris (4- hydroxyphenyl)-4-propyl-1H-pyrazol (PPT) replacement therapy at a dose of 10μg/rat/day for ten days.
•Group V: Was subjected to ovariectomy and a selective beta estrogen receptor agonist 2, 3-bis (4-Hydroxyphenyl) Propionitrile (DPN) replacement therapy at a dose of 10μg/rat/day for ten days. Each group is subdivided into three sub groups formed of 6 rats each.
Subgroup A: In which basal gastric acid secretion was measured and number of ulcers was counted.
Subgroup B: In which gastric acid was induced by Car-bamylcholine chloride (carbachol) 30μg/kg S.C. after three hours the stomach was removed, acid secretion was measured and number of ulcers was counted.
Subgroup C: Was subjected to indomethacin induced ulcer by oral administration of indomethacin 48mg/kg after three hours the stomach was removed, acid secretion was measured and number of ulcers were counted.
Results: Results showed that gastric acid secretion and number of ulcers were significantly higher among ovariecto-mized group than in control group when estimated within the basal acid secretion, carbachol induced acid secretion and indomethacin induced ulcer sub groups (p<0.05).
There was statistical significant increase in gastric acid secretion in the ovariectomized with estrogen replacement group as compared to the control group in basal acid secretion sub-group only (p<0.05). Also there was statistical significant increase in the number of ulcers in the ovariectomized with estrogen replacement sub-groups as compared to the control group (p<0.05), except for indomethacin induced ulcer sub group.
No significant difference had been observed between ovariectomized with alpha estrogen receptor agonist (PPT) sub-groups and the control group as regard acid secretion and number of ulcers (p 0.05).
Gastric acid secretion and number of ulcers were signif-icantly higher among ovariectomized with beta estrogen receptor agonist (DPN) group than in control group in basal acid secretion and carbachol induced acid secretion sub groups (p<0.05). While in indomethacine induced ulcer sub group the difference was not significant.
Also the results showed that gastric acid secretion and the number of ulcers were significantly lower among ovariec-tomized with estrogen replacement group and ovariectomized with alpha estrogen receptor agonist group compared with ovariectomized group in all studied sub groups (p<0.05).
The number of ulcers was significantly lower among ovariectomized with beta estrogen receptor agonist group than ovariectomized group in all studied sub groups (p<0.05). While Gastric acid secretion was significantly lower among ovariectomized with beta estrogen receptor agonist group compared with ovariectomized group in indomethacine induced ulcer sub group only (p<0.05).
There was no statistical significant difference between ovariectomized with estrogen replacement group compared with ovariectomized with alpha estrogen receptor agonist group and ovariectomized with beta estrogen receptor agonist group as regard acid secretion and number of ulcers. Except there was a significant lower number of ulcers in ovariecto-mized with alpha estrogen receptor agonist group as compared to ovariectomized with estrogen replacement group in the basal acid secretion and carbachol induced acid secretion sub-groups (p<0.05).
Conclusion: Our data indicate that estrogen decreases gastric acid secretion and number of peptic ulcers and this effect occur through stimulation of alpha and beta estrogen receptors.
This may provide an initial rationale for a potential hormone (estrogen) therapy to protect the GIT in postmeno-pausal women. Hence it is recommended to use estrogen replacement therapy in postmenopausal women to protect against gastric and duodenal ulcers.