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血管内皮生长因子C在子宫内膜异位症中的表达及抗血管生成治疗

Expression of vascular endothelial growth factor C and anti-angiogenesis therapy in endometriosis.

作者信息

Song Wei-Wei, Lu Huan, Hou Wen-Jing, Xu Guang-Xu, Zhang Ji-Hong, Sheng You-Hua, Cheng Ming-Jun, Zhang Rong

机构信息

Medical College of Soochow University Shanghai 215123, P. R. China ; Department of Obstetrics and Gynecology, Shanghai Jiaotong University Affiliated Sixth People Hospital South Campus Shanghai 201499, P. R. China.

Department of Obstetrics and Gynecology, Shanghai Jiaotong University Affiliated Sixth People Hospital South Campus Shanghai 201499, P. R. China.

出版信息

Int J Clin Exp Pathol. 2014 Oct 15;7(11):7752-9. eCollection 2014.

Abstract

Angiogenesis is an important pathogenesis of Endometriosis. Vascular endothelial growth factor C (VEGF-C) is one of the most important factor in the regulation of both normal and abnormal angiogenesis. Anti-angiogenic treatment of endometriosis is still in the exploratory stage. In this study, we investigate the relationship between VEGF-C and endometriosis, the therapeutic effects of Endostar in the rat endometriosis model. We then demonstrated that Immunohistochemical expression of VEGF-C was higher in endometriotic tissues than in control normal ovary tissues (P < 0.01) and higher in the endomertriosis grade III-IV than in endomertriosis grade I-II (P=0.013). In rat endometriosis model, we observed a significant reduction in the mean volume and weight of the endometriotic implants per rat in the treatment group as compared with the control group. By immunohistochemical evaluation, there was a significant reduction in VEGF-C expression after treatment in all areas examined. VEGF-C may be involved in the pathogenesis of endomertriosis by regulating the angiogenesis. Endostar has therapeutic effects of endometriosis lesions in the rat endometriosis model.

摘要

血管生成是子宫内膜异位症的重要发病机制。血管内皮生长因子C(VEGF-C)是调节正常和异常血管生成的最重要因子之一。子宫内膜异位症的抗血管生成治疗仍处于探索阶段。在本研究中,我们研究了VEGF-C与子宫内膜异位症之间的关系,以及恩度在大鼠子宫内膜异位症模型中的治疗效果。然后我们证明,VEGF-C在异位内膜组织中的免疫组化表达高于对照正常卵巢组织(P<0.01),在III-IV期子宫内膜异位症中高于I-II期子宫内膜异位症(P=0.013)。在大鼠子宫内膜异位症模型中,我们观察到与对照组相比,治疗组每只大鼠异位内膜植入物的平均体积和重量显著降低。通过免疫组化评估,在所有检查区域治疗后VEGF-C表达均显著降低。VEGF-C可能通过调节血管生成参与子宫内膜异位症的发病机制。恩度对大鼠子宫内膜异位症模型中的异位症病变有治疗作用。

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