Endostatin in the Treatment of the Transplanted Model of Endometriosis in SCID Mice

In: Journal of Practical Obstetrics and Gynecology · 2006 · W2352594364
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Recombinant human endostatin reduced endometriosis lesion volume and microvessel density in SCID mice by inhibiting angiogenesis and decreasing vascular endothelial growth factor expression.

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Abstract

Objective:To investigate the effects of recombinant human endostatin (YH-16) on focus development and angiogenesis of endometriosis (EMS).Methods:Eutopic endometrium from endometriosis was subcutaneously transplanted into SCID mice,and the EMs mice model was established.Then the mice were randomized into treatment group (n=10) received recombinant human endostatin YH-16 (2 mg/kg·d~ -1 ) by intraperitoneal injection;and the control group (n=10) received PBS as above.The treatment regimen lasted 14 days.The volumes of EMs lesion were observed every three days.Immunohistochemistry was used to determine microvessel density (MVD) and the expression of VEGF in ectopic tissue.Results:Compared with the control group,growth of endometriosis lesion was reduced in mice treated with YH-16.The differences were statistically significant for the weight and volume of ectopic lesion between the treatment group and the control group (P0.05).On light microscopy,atrophic gland,non-integrated structure,and some necrosis in stroma can be seen in YH-16 group.MVD and expression of VEGF decreased significantly in the group using YH-16 than the control group (P0.05).Conclusions:Recombinant human endostatin can effectively interfere with the maintenance and growth of endometriosis by inhibiting angiogenesis,and endostatin can reduce the expression of VEGF in ectopic lesion.This suggests that the use of angiostatic agents may be promising as a therapy for endometriosis.

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endometriosis

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