Apoptotic signaling pathways in uteri of rats with endometrial hyperplasia induced by ovariectomy combined with estrogen.

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.