Metformin regresses endometriotic implants in rats by improving implant levels of superoxide dismutase, vascular endothelial growth factor, tissue inhibitor of metalloproteinase-2, and matrix metalloproteinase-9

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Metformin treatment in rats led to regression of endometriotic implants by modulating key molecules involved in oxidative stress, angiogenesis, and extracellular matrix remodeling.

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Abstract

ObjectiveWe sought to test if metformin could regress endometriotic explants in rats.Study designAfter inducing endometriotic implants and randomization of female Wistar albino rats, they were given 25 and 50 mg/kg/day of oral metformin in group A (n = 9) and B (n = 8), respectively, for 28 days. Group C (n = 9) was given saline as placebo.ResultsMean volume, weight, and histologic score of implants in groups A (P < .01, P < .05, and P < .05, respectively) and B (P < .01, P < .05, and P < .05, respectively) were significantly lower than in group C. The activity of superoxide dismutase and tissue inhibitor of metalloproteinase-2 staining in groups A (P < .05 and P < .01, respectively) and B (P < .01 and P < .01, respectively) was significantly higher than in the control group. Moreover, there were more significant reductions in implant levels of vascular endothelial growth factor and matrix metalloproteinase-9 in groups A (both P < .001) and B (both P < .001) than in group C.ConclusionMetformin causes regression of endometriotic implants in rats.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Matrix Metalloproteinase 9 Metformin Superoxide Dismutase Tissue Inhibitor of Metalloproteinase-2 Vascular Endothelial Growth Factor A Animals Disease Models, Animal Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Female Hypoglycemic Agents Hypoglycemic Agents Immunohistochemistry Laparotomy

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