Effect of GnRH-II on the ESC proliferation, apoptosis and VEGF secretion in patients with endometriosis in vitro.
OBJECTIVE
To study the effect of GnRH-II on the cell proliferation, apoptosis and secreting vascular endothelial growth factor (VEGF) of ectopic, eutopic and normal endometrial stromal cells (ESC) from patients with or without endometriosis (EMs) in vitro.


METHODS
The ectopic, eutopic and normal ESC were isolated, cultured and identified, then added 0 M, 10(-10) M, 10(-8) M, 10(-6) M GnRH-II. The growth and proliferation of three ESC were measured by MTT assay; the cell apoptosis were detected with the method of Hoechst staining and Flow Cytometry test; ELISA was used to measure the VEGF concentration change by three ESC secretion.


RESULTS
GnRH-II inhibited the proliferation of ectopic, eutopic ESC from patients with endometriosis and normal ESC from control patients, in a dose- and time-dependent manner (P<0.05); GnRH-II increased the apoptotic rate of three ESC in a dose-dependent manner (P<0.05); The concentration of VEGF in three ESC was significantly decreased after the treatment of GnRH-II, in a dose-dependent manner (P<0.01); And these above effects were the strongest on the ectopic than on the eutopic or normal, there were statistical significance (P<0.05); and three was no significantly difference between the eutopic and normal (P>0.05).


CONCLUSIONS
GnRH-II significantly inhibited the cell proliferation, induced cell apoptosis and decreased the VEGF secreting of ectopic, eutopic and normal ESC in EMs in vitro, and these effects were the strongest on ectopic ESC, which suggested that GnRH-II may become a new effective treatment for endometriosis.
Departments of Obstetrics and Gynecology and Otorhinolaryngology, Second Xiangya Hospital, Central South University Changsha, Hunan, China, 410011.
Fengying
F
Huang
Huanping
H
Wang
Ying
Y
Zou
Qiuhong
Q
Liu
Jing
J
Cao
Tuanfang
T
Yin
D000328:Adult; D017209:Apoptosis / Q000187:drug effects*; D016022:Case-Control Studies; D049109:Cell Proliferation / Q000187:drug effects*; D048430:Cell Shape / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000494:pharmacology; D006801:Humans; D017154:Stromal Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D007987:Gonadotropin-Releasing Hormone; C047717:LHRH, His(5)-Trp(7)-Tyr(8)-
Endometriosis (EMs); cell apoptosis; cell proliferation; endometrial stromal cells (ESC); gonadotropin releasing hormone-II (GnRH-II); in vitro; vascular endothelial growth factor (VEGF)