title: Melatonin causes regression of endometriotic implants in rats by modulating angiogenesis, tissue levels of antioxidants and matrix metalloproteinases.
abstract: OBJECTIVE
  The aim of this study was to test if melatonin causes regression of endometriotic implants and whether it influences implant levels of superoxide dismutase (SOD), malondialdehyde (MDA), vascular endothelial growth factor (VEGF), tissue inhibitor of metalloproteinase (TIMP)-2 and matrix metalloproteinase (MMP)-9 in rats.
  
  
  METHODS
  Endometriotic implants were introduced surgically to 20 female Wistar albino rats, which were either treated with melatonin via intraperitoneal injection for four weeks (melatonin group, n = 10) or with saline (control group, n = 10) after a second-look laparotomies. The main outcome measures included volume (mm(3)) and weight (mg) of explants and tissue levels of SOD, MDA, VEGF, TIMP-2 and MMP-9.
  
  
  RESULTS
  Before and after treatment implant volumes of the melatonin group were decreased significantly (P < 0.01) while there was no significant difference between the pretreatment and posttreatment implant volumes of the control group. Moreover, weight (P < 0.05) and histologic score (P < 0.05) of implants of the melatonin-treated rats were significantly lower than controls. Activity of SOD and TIMP-2 staining in melatonin group was significantly higher (both P < 0.01) while there were significant reductions in implant levels of VEGF and MMP-9 in melatonin group (both P < 0.01) than controls.
  
  
  CONCLUSIONS
  Melatonin induces the regression of endometriotic implants in rats by modulating implant levels of SOD, MDA, VEGF, MMP-9 and TIMP-2.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, Izmir Katip Celebi University, Izmir, Turkey, drbulentyilmaz@yahoo.com.
authors.forename: Bulent
authors.initials: B
authors.lastname: Yilmaz
authors.forename: Sevtap
authors.initials: S
authors.lastname: Kilic
authors.forename: Orhan
authors.initials: O
authors.lastname: Aksakal
authors.forename: Ibrahim Egemen
authors.initials: IE
authors.lastname: Ertas
authors.forename: Gonca Gul
authors.initials: GG
authors.lastname: Tanrisever
authors.forename: Yasemin
authors.initials: Y
authors.lastname: Aksoy
authors.forename: Nese
authors.initials: N
authors.lastname: Lortlar
authors.forename: Sefa
authors.initials: S
authors.lastname: Kelekci
authors.forename: Tayfun
authors.initials: T
authors.lastname: Gungor
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D004195:Disease Models, Animal; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D007274:Injections, Intraperitoneal; D008315:Malondialdehyde / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D020782:Matrix Metalloproteinases / Q000378:metabolism*; D008550:Melatonin / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D000975:Antioxidants; D042461:Vascular Endothelial Growth Factor A; D019716:Tissue Inhibitor of Metalloproteinase-2; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D020782:Matrix Metalloproteinases; D020780:Matrix Metalloproteinase 9; D008550:Melatonin