Vitamin D3 promotes regression of endometrial implants comparable to buserelin in a rat model of endometriosis.

Buserelin, a gonadotropin-releasing hormone agonist, reduces gonadotropin and estrogen levels and is commonly used to alleviate the symptoms of endometriosis. Vitamin D3 has been reported to exhibit anti-inflammatory and pro-apoptotic properties, which may contribute to the regression of endometrial lesions. We aimed to investigate the effects of vitamin D3 on the regression and recurrence prevention of endometrial implant sites through the induction of apoptosis comparable to buserelin acetate in an experimental rat endometriosis model. Endometrial implant size and adhesion scores were evaluated following treatment. Microscopic analyses were performed using hematoxylin-eosin-stained preparations. Apoptotic activity was assessed by TUNEL assay, along with the expression of Bcl-2 and Bax antibodies. Untreated rats exhibited larger implant volumes, severe glandular and stromal alterations, and pronounced inflammatory infiltration. In contrast, vitamin D3 and buserelin treatments reduced implant size and adhesion scores. The vitamin D3-treated group demonstrated a high density of TUNEL-positive cells. Increased expression of Bcl-2 protein was found in untreated groups whereas, increased expression of Bax protein was found in both treated groups. In conclusion, vitamin D₃ may have contributed to the regression of endometrial implants, possibly through mechanisms involving apoptotic pathways. Further studies are needed to clarify its role and to evaluate its potential clinical relevance.