title: Apoptotic signaling pathways in uteri of rats with endometrial hyperplasia induced by ovariectomy combined with estrogen.
abstract: OBJECTIVE
  To explore a new reliable method inducing an animal model similar to the morphology and apoptotic signaling pathways in endometrial hyperplasia patients.
  
  
  METHODS
  After the rats were ovariectomized, estradiol benzoate (60 µg/​100 g) was intramuscularly injected on alternate days for 4 weeks. The morphology in the uterus was observed under a light microscope and by electron microscopy. The expression levels of survivin/caspase-3 and Fas/FasL were checked by immunohistochemistry, Western blotting and real-time polymerase chain reaction.
  
  
  RESULTS
  After the models were induced, the edema and hypertrophy in uteri were observed 4 weeks later. The glands in the endometrium had increased, indented hyperplasia of glandular cells appeared, and a pseudo-stratified phenomenon occurred. Under a transmission electron microscope, free ribosomes had markedly increased and the nucleus was enlarged in the cytoplasm. Compared with the control group, the expression of survivin increased (p < 0.05) while that of caspase-3 and Fas/FasL declined (p < 0.05).
  
  
  CONCLUSIONS
  In the rat model of endometrial hyperplasia induced by ovariectomy with pharmacological estrogen add-back treatment, survivin, caspase-3 and Fas/FasL signaling pathways play an important role in regulating the apoptosis of glandular cells in uteri.
authors.affiliation: Department of Clinical Medicine, Shaanxi University of Traditional Chinese Medicine, Xi'an, China. Hefengjie@yahoo.cn
authors.forename: Fengjie
authors.initials: F
authors.lastname: He
authors.forename: Wenting
authors.initials: W
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D004247:DNA / Q000737:chemistry / Q000235:genetics; D004195:Disease Models, Animal; D004714:Endometrial Hyperplasia / Q000473:pathology*; D004958:Estradiol / Q000008:administration & dosage / Q000031:analogs & derivatives; D053222:Fas Ligand Protein / Q000235:genetics / Q000378:metabolism; D005260:Female; D007150:Immunohistochemistry; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D010052:Ovariectomy; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction; D013047:Specific Pathogen-Free Organisms; D000077022:Survivin; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: C516989:Birc5 protein, rat; D053222:Fas Ligand Protein; C491898:Fas protein, rat; D008869:Microtubule-Associated Proteins; D000077022:Survivin; D019014:fas Receptor; C074283:estradiol 3-benzoate; D004958:Estradiol; D004247:DNA; D053148:Caspase 3