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Effects of Estradiol and Progesterone on Gastric Mucosal Response to Early Helicobacter pylori Infection in Female Gerbils
Author(s) -
SaquiSalces Milena,
RochaGutiérrez Brenda L.,
BarriosPayán Jorge A.,
RuizPalacios Guillermo,
CamachoArroyo Ignacio,
GamboaDominguez Armando
Publication year - 2006
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2006.00386.x
Subject(s) - gastrin , medicine , proliferating cell nuclear antigen , endocrinology , tunel assay , ovariectomized rat , helicobacter pylori , gastritis , estrogen , atrophy , gastric mucosa , immunohistochemistry , biology , follicular phase , atrophic gastritis , apoptosis , secretion , stomach , biochemistry
Background: Gender differences have been shown regarding the changes in the inflammatory response, gastrin secretion, and gastric acidity during Helicobacter pylori infection. Aim: To investigate the role of estradiol and progesterone in the changes of the gastric mucosa induced by H. pylori during the early stage of infection in female gerbils. Materials and Methods: Thirty‐three adult ovariectomized female gerbils were infected with H. pylori (SS1); 7 days after infection they were treated with low and high doses of estradiol (50 and 250 µg/60 days pellet), progesterone (15 and 50 mg/60 days pellet) and vehicle. Non‐ovariectomized infected gerbils were used as control. Gerbils were euthanized after 6 weeks of infection. Histologic evaluation, immunohistochemical detection of proliferation cell nuclear antigen (PCNA), gastrin, and apoptosis by terminal deoxynucleotide nick end labeling (TUNEL) assay were performed. Positive cells for PCNA, TUNEL, and gastrin were counted in 10 oriented glands per animal. Two‐sided p = .05 was considered significant. Results: Estradiol‐treated groups showed more intense and extended acute and follicular gastritis compared to the vehicle group, whereas progesterone‐treated groups presented less gastritis than the other groups. Proliferation and apoptosis indexes were significantly lower in the vehicle group when compared with those of the control; both indexes were increased in the high‐dose estradiol and progesterone groups as compared with those of the vehicle. Grade I nonmetaplastic atrophy was observed in the vehicle and progesterone groups. The high‐dose progesterone group showed a significant reduction in the number of gastrin cells. Conclusions: Estradiol and progesterone participate in the gastric mucosal response to early H. pylori infection in gerbils.