Effect and mechanism of formation of intrauterine adhesion at different dose of estrogen
10.3760/cma.j.issn.0529-567x.2010.12.009
- VernacularTitle:不同水平雌激素在宫腔粘连形成中的作用及相关机制
- Author:
Fang CHEN
;
Hua DUAN
;
Ying ZHANG
;
Yanhua WU
- Publication Type:Journal Article
- Keywords:
Estrogens;
Uterus;
Adhesions;
Endometrium;
Fibrosis;
Transforming growth factor beta 1;
Fibroblast growth factor 2
- From:
Chinese Journal of Obstetrics and Gynecology
2010;45(12):917-920
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of the formation of intrauterine adhesion (IUA) at different dose of estrogen. Methods Thirty-three New Zealand female rabbits were randomly divided into low estrogen group, normal physiological estrogen group, moderate estrogen group and high estrogen group. Animals of the low, moderate and high groups were ovariectomized (OVX) while normal group underwent sham operation. The moderate and high group animals received 0. 5 mg or 1.0 mg estradiol benzoate after OVX twice a week respectively. Two weeks later, all animals received curettage under direct vision. Serum was collected regularly to determine levels of estradiol (E2), transforming growth factor β1 (TGF-β1) and basic fibroblast growth factor (bFGF). Two weeks after curettage, we cut open cavity to collected endometrium for HE and Masson staining to score extent of endometrial fibrosis and IUA.Results The score of extent of endometrial fibrosis in high group (6. 1 ± 1.5) was higher than those in low estrogen group, normal estrogen group, moderate estrogen group (2. 7 ± 2. 1, 1.2 ± 1.8, 2. 7 ± 2. 0; all P <0. 05). The score of extent of IUA in high group (4. 0 ±2. 5) was higher than that in any other groups (0. 3 ± 0. 8, 1.0 ± 1.6, 1.7 ± 1.9; all P < 0. 05). The levels of TGF-β1 and bFGF was correlated with the level of E2 positively (P < 0. 01) and they had positive relationship with extent of endometrial fibrosis and IUA (P <0. 05). Conclusion High estrogen could accelerate endometrial fibrosis and IUA by promoting expression of TGF-β1, bFGF.
