Aim: To explore the role of microenvironment of peritoneal fluid in pathogenesis of endometriosis, the source and its regulation in peritoneal fluid.
Methods: Peritoneal Mphis from 14 patients with endometriosis (endometriosis group)and 10 normal women ( control group) were cultured in vitro. Either 17-l estradiol, progesterone and LPS or their combinant were added to cultured peritoneal Mos from control group. VEGF levels in culture supernatant of M(Ds from two groups were detected by ELISA. Culture supernatant of serum-free media in two groups were added to the cultured endothelial cells. Effect of the supernatant on endothelial cell proliferation activity was examined by MTT colorimetry at wavelength of 450 nm. The expressions of Fit-1 and Flt-4 on the Mos from two groups were determined by immunohistochemical staining.
Results: The VEGF level in culture supernatant of Mps from endometriosis group was significantly higher than that from control group (P < 0. 05 ), and had no cyclic variation (P > 0. 05). As compared with LPS, estrogen and progentrogen could elevate notably the level ofVEGF secreted by Ms ( P < 0. 05 ). However, the regulation of MWs secreted VEGF level by estrogen and progestoron had no marked difference. The Mos activated by LPS could strengthen the regulation of VEGF secreted by Mphis under estrogen and progestron stimulation. Culture supernatant of serum-free media for Mos could promote significantly the proliferation of endothelial cells ( P < 0. 05 ). Fit-land Flt-4 on Mos was expressed without cyclic variation (P>0.05).
Conclusion: The VEGF may be secreted by Mos in peritoneal fluid of endometriosis group. The endothelial cell proliferation and angiogenesis are enhanced by change of microenvironment of peritoneal fluid.