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目的研究促性腺激素释放激素(gonadotropin-releasing hormone,GnRH)及其受体(gonadotropin-releasing hormone receptors,GnRH-R)在卵巢子宫内膜异位症(endometriosis,EM)与子宫腺肌病(adenomyosis,AM)在位、异位组织中的表达及临床意义。方法选取2010年3月至2011年5月内蒙古医科大学附属医院和包头市包钢职工医院来源的42例EM,34例AM及20例正常子宫内膜组织,经石蜡包埋制备病理切片,应用免疫组织化学方法检测GnRH及GnRH-R蛋白表达情况。结果 (1)AM与EM组的在位内膜中,GnRH和GnRH-R持续表达。(2)EM组的异位内膜GnRH和GnRH-R的阳性率低于在位内膜及对照组,差异有统计学意义(P<0.05)。在位子宫内膜的阳性表达率高于正常子宫内膜,差异有统计学意义(P<0.05),而异位内膜低于正常子宫内膜,差异有统计学意义(P<0.05)。(3)AM组异位内膜GnRH和GnRH-R的阳性率低于在位内膜表达率,差异有统计学意义(P<0.05)。AM组在位子宫内膜的阳性表达率高于正常子宫内膜,差异有统计学意义(P<0.05),而异位内膜与正常子宫内膜相比,差异无统计学意义(P>0.05)。(4)AM、EM及对照组的GnRH和GnRH-R在月经周期在位内膜的表达均为分泌期高于增生期,差异有统计学意义(P<0.05)。结论 GnRH可能通过其受体介导,对异位内膜的种植和生长产生抑制作用,为临床应用GnRH类似物及GnRH拮抗剂治疗这两种疾病提供理论依据。
Objective To investigate the effect of GnRH and its receptor (GnRH-R) on the pathogenesis of ovarian endometriosis (EM) and adenomyosis (Adenomyosis) , AM) in ectopic tissues and their clinical significance. Methods From March 2010 to May 2011, 42 cases of EM, 34 cases of AM and 20 cases of normal endometrium from the Inner Mongolia Medical University Hospital and Baotou Workers’ Hospital of Baotou City were selected. Pathological sections were prepared by paraffin embedding. Immunohistochemistry was used to detect the expression of GnRH and GnRH-R protein. Results (1) GnRH and GnRH-R were continuously expressed in the eutopic endometrium of AM and EM groups. (2) The positive rate of GnRH and GnRH-R in ectopic endometrium in EM group was lower than that in eutopic endometrium and control group, with significant difference (P <0.05). The positive rate of eutopic endometrium was higher than that of normal endometrium (P <0.05), while the ectopic endometrium was lower than that of normal endometrium (P <0.05). (3) The positive rates of GnRH and GnRH-R in ectopic endometrium in AM group were lower than those in eutopic endometrium, the difference was statistically significant (P <0.05). The positive expression rate of eutopic endometrium in AM group was higher than that in normal endometrium (P <0.05), while there was no significant difference between ectopic endometrium and normal endometrium (P> 0.05). (4) The expressions of GnRH and GnRH-R in AM, EM and control groups in the eutopic and eutopic endometrium of the menstrual cycle were both higher than the proliferative phase (P <0.05). Conclusions GnRH may be mediated through its receptor, which can inhibit the growth and implantation of ectopic endometrium, and provide a theoretical basis for the clinical application of GnRH analogues and GnRH antagonists in the treatment of these two diseases.