Vascular Endothelial Growth Factor In Peritoneal Fluid Research Articles

Sulforaphane Attenuates Endometriosis in Rat Models Through Inhibiting PI3K/Akt Signaling Pathway.

Sulforaphane exerts anti-inflammatory activity in inflammatory diseases. The endometriosis (EM) is accompanied by chronic inflammation. The present study aims to explore the therapeutic effects of sulforaphane on EM and its underlying mechanism. An EM rat model was established by transplantation of autologous fragments. The rats were intragastrically administered sulforaphane (5 mg/kg, 15 mg/kg, and 30 mg/kg) for 3 weeks. The volumes of endometriotic foci and adhesion score were calculated at the end of the experiment. Levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and vascular endothelial growth factor (VEGF) were determined by enzyme-linked immunosorbent assay (ELISA). Expressions of VEGF, B-cell lymphoma/leukemia 2 (Bcl-2), Bax, cleaved caspase-3, PI3K, and Akt in endometrial tissue were determined by Western blotting. Relative expressions of PI3K and Akt were determined by quantitative polymerase chain reaction. Posttreatment of sulforaphane dose-dependently decreased the volumes of endometriotic foci and adhesion score in EM model. Additionally, posttreatment of sulforaphane inhibited levels of IL-6, IL-10, TNF-α, IFN-γ, and VEGF in peritoneal fluid and plasma. Posttreatment of sulforaphane regulated the expressions of VEGF, bcl-2, Bax, and cleaved Caspase-3 in EM model. The underlying mechanism revealed that sulforaphane attenuated EM in the rat model by inhibition of PI3K/Akt signaling pathway.

The Non-Ergot Derived Dopamine Agonist Quinagolide as an Anti-Endometriotic Agent

Aim: The study aimed to investigate the efficacy of a dopamine agonist, quinagolide, on experimentally induced endometriosis in a rat model. Methods: Twenty female Wistar rats were used in this experiment. Endometriosis was surgically induced by transplantation of autologous endometrial tissue. A second laparotomy was performed 4 weeks after the first one to assess the pre-treatment implant volumes, and peritoneal lavage with saline solution was performed to assess the peritoneal cytokine levels. Rats were randomized to treatment with quinagolide or saline. At the end of the treatment period, a third laparotomy was performed to compare pre- and post-treatment implant volumes and cytokine levels within the groups. Implants were excised to compare glandular tissue (GT) and stromal tissue (ST) scores between the groups. Results: In the quinagolide group, post-treatment volume was statistically significantly reduced compared with pre-treatment volume (p = 0.01). There were significant decreases in interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) levels in peritoneal fluid samples in quinagolide-treated rats when compared to pre-treatment levels (p = 0.03 and p < 0.01). Histopathologically, both GT and ST scores were significantly lower in the quinagolide group compared to the control group (p = 0.01 and p = 0.02). Conclusions: Quinagolide caused a significant regression in endometriotic implants and it also significantly reduced the levels of IL-6 and VEGF in peritoneal fluid.

Elevated vascular endothelial growth factor (VEGF) and active and latent transforming growth factor-β (TGF-β) in the peritoneal fluid of women with pelvic adhesions and with endometriosis.

Objective: To evaluate TGF-b and VEGF concentrations in the peritoneal fluid of women with pelvic adhesions and with endometriosis. Design: Descriptive study. Materials/Methods: Patients in a university teaching hospital. Reproductive age women undergoing laparoscopy for pelvic pain or infertility. Aspiration of the peritoneal fluid during laparoscopy. Determination of the concentrations of active TGF-b, latent TGF-b and VEGF in peritoneal fluid. Results: The total (active and latent) TGF-b levels were significantly higher in women with adhesions (201.6 ± 27.6 pM) and endometriosis (196.8 ± 32.5 pM) compared to women without endometriosis and adhesion (control group, 108.0 ± 14.4 pM). Similarly, VEGF levels were significantly higher in women with pelvic adhesions (683.7 ± 81.4 pg/mL) and endometriosis (346.5 ± 124.1 pg/mL) compared to the control group (64.1 ± 8.3 pg/mL). More interestingly, the concentrations of VEGF and biologically active TGF-b in the adhesion group were higher than in the endometriosis group. Conclusions: The concentrations of TGF-b (both bioactive and latent) and VEGF are elevated in the peritoneal fluid of women with pelvic adhesions and with endometriosis. Also, bioactive TGF-b and VEGF levels in the adhesion group are higher than in the endometriosis group. The enhanced expression of VEGF and the increased expression and activation of TGF-b in the peritoneal fluid of women with endometriosis or post-surgical adhesions suggest that these growth factors play a role in the pathogenesis of these conditions. Whether women with elevated peritoneal fluid concentrations of active or latent TGF-b and VEGF are prone to develop adhesions remains to be determined. Supported by: McGill University.