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Abstract Objective: To observe the effect of mifepristone on the expression of Fas and Fas ligand (FasL) in endometrial hyperplasia of rats, and to explore the therapeutic mechanism of endometrial hyperplasia. Method: Forty-five SD rats were included, of which 15 rats were randomly selected as normal control, and the other 30 were treated to be a rat model of endometrial hyperplasia with "estrogen load method". The model rats were randomly divided into mifepristone group (n=15) with intragastric administration of mifepristone suspension for 4 weeks and disease model group (n=15) with intragastric administration of normal saline at the same volume for 4 weeks. Expression levels of Fas and FasL were evaluated by immunohistochemistry method. Results: The expression level of Fas protein (146.90±24.12) in the model group was significantly lower than that in normal control group (116.63±16.94, P<001). There were no significant differences between the mifepristone group and the normal group(P＞0.05). The expression level of FasL protein in the model group (122.77±28.10) was significantly lower than that of normal control group (149.75±29.53, P<0.01). The expression level of FasL protein was (132.50±27.97), higher than that of the model group (P>0.05), but lower than that of the normal group (P>0.05). Conclusion: Abnormal apoptosis mediated by decreased expression level of Fas and increased expression level of FasL plays an important role in the pathogenesis of endometrial hyperplasia. Mifepristone could up-regulate the expression of Fas in endometrial tissue and inhibit the excessive expression of FasL. Presumably one of mechanism of the treatment of endometrial hyperplasia is possibly inhibit the endometrial hyperplasia by restoring the apoptosis balance of endometrial epithelial cell.
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