The Function Of Estrogen On The Proliferative Mechanism Of Children Hemangioma And Its Clinical Significance

Objective: To study the promotion mechanism of angiogenesis of children hemangioma, to clarify the angiogenesis function of estrogen on the proliferative mechanism of children hemangioma, and also to provide the new theoretical evidence for ant-estrogen drugs cured children hemangioma.Mothod: Expression and relativity of estrogen receptor(ER), VEGF and bFGF were detected with SP immunohistochemical method in 42 specimens of hemangioma and 17 specimens of vascular malformation. A fragment of hemangioma biopsy was embedded in fibrin gel, and a in vitro human model of angiogenesis of hemangioma was founded. The angiogenesis of hemangioma fragments of each group was interfered by estrogen and tomaxifen, and the dimension of newborn tubule area in the 3rd, 6th, 9th day after culture was calculated to compare statistically significant differences among the groups.Result:1. The label index (LI) of ER, VEGF and bFGF in the hemangioma weresignificantly higher than those in the vascular malformation(p<0.01) and in the hemangioma the LI of ER. VEGF and bFGF inproliferative stage were higher than those in involutingstage(p<0.01). There were significantly positive correlations between the LI of ER and VEFG, bFGF strong in hemangioma and weakin the vascular malformantion(p<0. 05).2. In the model of angiogenesis of hemangioma, microvessels grew out from the tissue fragments in 2nd to 3th day after culture, and in 8th to 9th day a complex network of microvessels come to being, the tending to inactivity. The complex network around the tissue fragments was confirmed to he vascular by immunohistochemistry experimentation and electron microscopic observation.3. In the 3rd, 6th and 9th day after culture the dimension of newborn tubule area of the group of estrogen were significantly larger than those of the group of control. Those of the group of estrogen +tomaxifen and the group of tomaxifen were significant smaller than those of the group of estrogen and the group of control. (p<0. 05)Conclusion:1. Through the experimentation of immunohistochemistry and the study of culture in vitro it is demonstrated that estrogen stimulates angiogenesis of children hemangioma. The mechanism is possibly that estrogen bound to estrogen receptor leads to raise the expression of VEGF and bFGF, and/or cooperate with VEGF and bFGF to stimulate angiogenesis. Tomaxifen can hold back this process.2. The model of angiogenesis of hemangioma provides a good model of researching the regulation mechanism of angiogenesis of hemangioma, and help to study the drugs of ant-estrogen and ant-angiogenesis toprovide a new approach for medication for children hemangioma.