The effect of tinzaparin sodium and leuprolide acetate in an experimental mouse model of endometriosis: The rol of the WNT/beta-catenin pathway

Objective Endometriosis is a benign condition driven by estrogen and inflammation in which endometrial-like tissue develops in ectopic locations. We aimed to determine whether non-steroidal agents acting on the WNT/beta-catenin signaling axis could provide therapeutic benefit in this disease.

Materials and Methods Forty adult female mice underwent surgical creation of endometriotic implants and were then distributed into five experimental arms: untreated controls, early leuprolide (leup1d), early tinzaparin (tnz1d), delayed leuprolide (leup7d), and delayed tinzaparin (tnz7d). Early treatment groups received drug treatment beginning at postoperative hour 24, whereas delayed groups began treatment on postoperative day 8. At two weeks post-surgery, lesions were harvested for RNA extraction and transcript profiling. Tissues were also processed for hematoxylin-eosin staining with semi-quantitative grading. Immunostaining was performed using antibodies against HIF1a and WNT2.

Results The tnz7d group exhibited decreased inflammatory markers, while the leup7d group displayed reduced epithelial content; both changes resulted in lower disease severity scores. WNT2 and HIF1a immunostaining revealed greater reductions in score in the tnz7d group compared with controls and other treatment arms, but these differences were not statistically significant.

Conclusion Further investigation is warranted to determine how tinzaparin sodium and leuprolide acetate modulate the WNT/β-catenin axis for the management of endometriosis.