Background and aim: Allopurinol is traditionally recommended for treatment of gout. The current study was planned to discover the influence and mechanism of allopurinol on endometrial hyperplasia (EH).
Experimental design: 24 female Wistar rats were classified into 3 groups. Control group: Rats were received carboxymethyl cellulose 1% orally. Endometrial hyperplasia group: Rats administered estradiol valerate (EV). Therapeutic group: Rats treated with allopurinol.
Results: In the EH group, there was significantly elevated serum uric acid and dyslipidemia. Also, significant elevation in NO and MDA tissue levels and significant reduction in tissue level of CAT, SOD, and Nrf2. Furthermore, tissue IL10 was significantly decreased while IL6, TNF-α, and NF-κB were significantly increased. Uterine PI3K, AKT, and mTOR genes were up-regulated. Histologically, there was increased endometrial thickness, stratification, numerous invaginations, and papillary formation of surface epithelium. Surface and glandular epithelium of endometrium revealed loss of BAX expression. All of the previously mentioned biochemical and histological alterations caused by estradiol-induced endometrial hyperplasia were reversed by allopurinol.
Conclusion: Therefore, these results revealed that allopurinol could suppress endometrial hyperplasia by targeting PI3K/AKT/mTOR and BAX signaling. In addition to its antioxidant and anti-inflammatory properties.