Open AccessThe expression of vascular endothelial growth factor is affected by hypoxia inducible factor-1α in peritoneum of endometriosis mice treated with genistein
Author(s) -
Sylvi Wafda Nur Amellia,
Yuyun Yueniwati,
Sutrisno Sutrisno
Publication year - 2016
Publication title -
middle east fertility society journal/middle east fertility society journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.322
H-Index - 18
eISSN - 2090-3251
pISSN - 1110-5690
DOI - 10.1016/j.mefs.2015.12.005
Subject(s) - endometriosis , genistein , vascular endothelial growth factor , angiogenesis , medicine , immunohistochemistry , peritoneum , hypoxia inducible factors , vegf receptors , hypoxia (environmental) , neovascularization , endocrinology , andrology , cancer research , biology , pathology , chemistry , biochemistry , organic chemistry , oxygen , gene
This study aimed to investigate whether the genistein is able to decrease the expressions of vascular endothelial growth factor-A (VEGF-A) and hypoxia inducible factor-1α (HIF-1α) in mouse model of endometriosis. Forty female mice (Mus musculus) were divided into eight groups (n = 5 each), including the control (untreated) group, endometriosis group, and endometriosis groups treated with various doses of genistein (50; 100; 200; 300; 400; and 500 mg/day). VEGF-A and HIF-1α analyses were performed by immunohistochemistry. We found significant increases in the VEGF-A and HIF-α expressions in endometriosis group compared to the control group. The increased expressions of VEGF-A and HIF-1α were significantly (p < 0.05) attenuated by the administration of all doses of genistein. In conclusion, in mouse model of endometriosis, genistein potentially inhibits the increase in angiogenesis in peritoneal tissue. Therefore, this result may provide a novel anti-angiogenic treatment strategy for the therapy of endometriosis