Department of Obstetrics and Gynecology.
Postgrad Med. 2014 Jan;126(1):104-10. doi: 10.3810/pgm.2014.01.2730.
The exact pathogenesis of endometriosis has not been completely discerned. 1-alpha,25-dihydroxyvitamin D3 (1,25[OH][2]D[3]) has been shown to have an anti-angiogenic effect and extracellular matrix-proteases-degrading properties. We hypothesized that 1,25(OH)(2)D(3) may have therapeutic value in the treatment of endometriosis.
Endometrial tissue was implanted into the abdominal peritoneum of 21 Wistar albino rats; the rats were randomized into 3 groups. In Group A (simultaneous group), we simultaneously induced endometriosis and began 1,25(OH)(2)D(3) treatment. Group B rats (sequential group) were treated after endometriosis was documented. Animals in Group C (control group) were followed without any treatment after the development of endometriosis.
Histologic score, mean volume, and weight of the explants in Group A and B were found to be significantly lower than those of the control group. Levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) immunoreactivities in Group A and B were also significantly lower compared with Group C. In contrast, intensities of immunoreactivity staining for tissue inhibitor of metalloproteinase-2 (TIMP-2) in Group A and B were significantly higher than that of the control group.
1,25(OH)(2)D(3) regresses endometriotic implants in rat models by altering implant levels of VEGF, TIMP-2, and MMP-9.
子宫内膜异位症的确切发病机制尚未完全阐明。1-α，25-二羟维生素 D3（1，25[OH] [2] D [3]）已显示出具有抗血管生成作用和细胞外基质蛋白酶降解特性。我们假设 1，25（OH）（2）D（3）在子宫内膜异位症的治疗中可能具有治疗价值。
将子宫内膜组织植入 21 只 Wistar 白化大鼠的腹腔腹膜中；将大鼠随机分为 3 组。在 A 组（同时组）中，我们同时诱导子宫内膜异位症并开始使用 1，25（OH）（2）D（3）治疗。B 组大鼠（序贯组）在记录子宫内膜异位症后进行治疗。C 组（对照组）动物在发展为子宫内膜异位症后不进行任何治疗而进行随访。
A 组和 B 组的组织学评分、平均体积和植入物重量明显低于对照组。A 组和 B 组血管内皮生长因子（VEGF）和基质金属蛋白酶-9（MMP-9）免疫反应水平也明显低于 C 组。相比之下，A 组和 B 组组织抑制剂金属蛋白酶-2（TIMP-2）的免疫反应染色强度明显高于对照组。
1，25（OH）（2）D（3）通过改变 VEGF、TIMP-2 和 MMP-9 在子宫内膜异位症植入物中的水平来使子宫内膜异位症在大鼠模型中消退。
