The protective effects of Azilsartan against hypoxia in endometrial stromal cells: an implication in endometriosis

Hua Chen, Cailing Han, Liyun Ren, Fang Wang, Jiao Cui, Chunfang Ha
In: Archives of Medical Science · 2022 · doi:10.5114/aoms/151804 · W4285793960
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Azilsartan treatment prevented the development of endometriosis in rats and inhibited hypoxia-induced endometrial stromal cell proliferation, migration, and invasion by downregulating HIF-1α/COX-2/PGE2 signaling.

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Abstract

Introduction Endometriosis is a reproductive disorder closely associated with hypoxia stress. Increasing evidences have implied the important roles of angiotensin II (ANG II) receptors in the pathophysiology of endometriosis. Thus, we speculated that Azilsartan (AZL), an ANG II receptor blocker, might have an effective function in controlling endometriosis. Material and methods The endometriotic animal model was established in female SD rats (6-8 weeks old, 200-220 g). Rats were divided into sham group and endometriosis (EMS) group. Rats in EMS group were anaesthetized by halothane and a mid-ventral incision was performed to expose the bowels. Human endometrial stromal cell line T-HESC was used for the in vitro assays. The T-HESC cells were cultured in DMEM-F12 mediumwith 10% fetal bovine serum (FBS, Hyclone), and 4 mM L-glutamine, 0.25% HEPES plus necessary antibiotics (Sigma-Aldrich, USA), at 37°C in a humidified atmosphere of 5% CO2. Results The results show that upregulation of ANG II type 1 (AT1) receptor was observed in the endometriotic rat models. Treatment with AZL prevented the development of endometriotic lesions and suppressed the expressions of HIF-1α and cyclooxygenase 2 (COX-2) in endometriotic rats. In vitro assays proved that hypoxia-induced proliferation, migration, and invasion of T-HESC cells were attenuated by AZL. AZL inhibited the expression levels of hypoxia-inducible factor-1α (HIF-1α), COX-2, and prostaglandin E2 (PGE2) production in hypoxia-induced T-HESC cells. Overexpression of HIF-1α blocked the effects of AZL on T-HESC cells in response to hypoxia. Conclusions AZL showed therapeutic function on endometriosis through inhibiting hypoxia-induced cell proliferation, migration, and invasion of T-HESC cells via HIF-1α/COX-2/PGE2 signaling.

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endometriosis

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