Estetrol Inhibits Endometriosis Development in an In Vivo Murine Model

Abstract

Endometriosis is characterized by the growth of endometrial-like tissue outside the uterus, and it is associated with alterations in the expression of hormone receptors and inflammation. Estetrol (E4) is a weak estrogen that recently has been approved for contraception. We evaluated the effect of E4 on the growth of endometriotic-like lesions and the expression of TNF-α, estrogen receptors (ERs), and progesterone receptors (PRs) in an in vivo murine model. Endometriosis was induced surgically in female C57BL/6 mice. E4 was delivered via Alzet pump (3 mg/kg/day) from the 15th postoperative day for 4 weeks. E4 significantly reduced the volume (p p 4 did not affect cell proliferation (PCNA immunohistochemistry) but it did increase cell apoptosis (TUNEL assay) (p p p p Esr2 reduced (p Esr1 (p Pgr (p 4 limited the development and progression of endometriosis in vivo.

Keywords

• endometriosis
• estetrol
• apoptosis
• proliferation
• hormone receptors
• oxidative stress