Effect of recombinant human endostatin on endometriosis in mice.
- Author:
Hong-Qing JIANG
1
;
Ya-Li LI
;
Jie ZOU
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Angiogenesis Inhibitors; therapeutic use; Animals; Disease Models, Animal; Endometriosis; drug therapy; pathology; physiopathology; Endometrium; blood supply; Endostatins; therapeutic use; Female; Humans; Mice; Mice, SCID; Middle Aged; RNA, Messenger; analysis; Recombinant Proteins; therapeutic use; Vascular Endothelial Growth Factor A; analysis; genetics
- From: Chinese Medical Journal 2007;120(14):1241-1246
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDDirect and indirect evidences have suggested that angiogenesis is a prerequisite for the development of endometriosis. Aiming at offering experimental evidences for anti-angiogenesis therapy, we transplanted the eutopic endometrium from patient with endometriosis into the severe combined immunodeficiency disease (SCID) mice, to evaluate the effect of the endostatin on the growth and angiogenesis of the established endometriosis lesions in SCID mice model.
METHODSEutopic endometrium of women with endometriosis was transplanted into the SCID mice. The mice were randomized into treatment (n = 10) and control groups (n = 10). Two weeks after the implantation of endometrium fragment, the treatment group was injected with recombinant human endostatin YH-16 into the peritoneal cavity (2 mgxkg(-1)xd(-1)), whereas the control group received equivalent volume of PBS (200 microl/d). The volume of endometriotic lesions in SCID mice was measured every three days, and all the treatment lasted for 14 days. Immunohistochemistry was used to determine microvessel density (MVD) and the expression of VEGF. The results were analyzed by t test and chi(2) test to value the treating effect.
RESULTSCompared with the control group, growth of endometriosis lesion was reduced in the mice treated with YH-16. Statistically significant differences in the volume and weight of the ectopic lesions were observed between the treatment and the control groups (P < 0.05). Microscopical examination showed that after being treated with YH-16, the volume of the endometrial tissues decreased, the glands depauperated, and the glandular epithelium partially degenerated. Necrotic debris was observed in the endometrial stroma. MVD and expression of VEGF in the treatment group were significantly lower than those in the control group (P < 0.05).
CONCLUSIONSRecombinant human endostatin affects the maintenance and growth of endometriotic tissues by inhibiting angiogenesis and reducing the expression of VEGF in ectopic lesion. The angiostatic agent may be promising as a therapy for endometriosis.