Search

Abstract This study aimed to analyze galectin-3 importance in endometriotic lesions development and the effect of recombinant Gal-3 carbohydrate recognition domain (Gal3C) in experimental endometriosis treatment. Experimental endometriosis was induced in WT and Gal-3−/− mice. Initially developed lesions were macroscopically and histologically analyzed, including immunohistochemical analysis. Then, WT mice were treated with Gal3C for 15 days. Gal-3 deficiency and Gal3C treatment significantly impaired endometriosis development. A significant decrease in lesions implantation and size, VEGF and VEGFR-2 expression, vascular density and macrophage distribution were observed in Gal-3 absence or inhibition. A greater presence of iNOS positive cells was observed in knockout mice lesions, while the presence of Arginase positive cells was higher in the WT animal lesions. In addition, COX-2 and TGFb1 were reduced by Gal3C treatment. Data showed here indicate a relevant role of Gal-3 in endometriosis development and highlight a target of endometriosis treatment using Gal-3 inhibitor. Highligths • Gal-3 absence or inhibition leads to impaired endometriotic lesions development. • Angiogenic markers and vascular density are decreased in Gal-3 absence/inhibition. • Macrophage population is reduced in Knockout or Gal3C treated endometriotic lesions. • Macrophage are majority iNOS positive in Gal-3 absence. [ABSTRACT FROM AUTHOR]

Objectives The hormonal treatment for endometriosis frequently fails to completely eradicate endometriotic implants. A new therapeutic treatment is needed. This study investigates the in-vitro effect of Copaifera langsdorffii oil-resin on human eutopic and ectopic endometrium stromal cell cultures (EuESCs and EctESCs). Methods A nanocomposite system containing the copaiba oil-resin (NanoCOR) was developed and acute toxicity test was performed. Endometrial stromal cells (ESCs) from non-endometriotics controls (CESCs), EuESCs and EctESCs were isolated and treated with different concentrations of NanoCOR, at different time intervals to evaluate its effect on cell morphology, proliferation, viability, necrosis and apoptosis induction. Key findings When treated with 50 µg/ml of NanoCOR, the morphology of EctESCs changed, as the actin microfilaments were disorganized, disassembled or disrupted. Moreover, at 24 h of treatment with NanoCOR, the EctESCs viability was inhibited, and a significant number of these cells underwent apoptosis. In EuESCs, these effects were observed only at 48 h. Finally, the treatment of EctESCs with NanoCOR increased the lactate dehydrogenase release into the extracellular medium more than in EuESCs. Conclusions Our data indicate that NanoCOR has a greater impact on the behaviour of human endometriotic stromal cells than on the eutopic endometrium stromal cells, supporting the idea that NanoCOR should be further investigated as a novel and valuable alternative to treat endometriosis. [ABSTRACT FROM AUTHOR]