论文部分内容阅读
目的:探讨促性腺激素释放激素激动剂(GnRHa)对腺肌病模型小鼠种植窗期内膜容受性的影响。方法:新生ICR小鼠滴喂他莫西芬建立子宫腺肌病模型,随机分为GnRHa降调的模型鼠组(A组)、模型对照鼠组(B组),并取同龄正常小鼠作为对照组(C组),每组8只,于100~115日龄处死,HE染色检测小鼠子宫病理变化;免疫组织化学CD31染色计算小鼠子宫微血管密度;免疫组织化学法检测种植窗期子宫内膜LIF表达及扫描电镜下观察胞饮突发育情况。结果:①口服他莫西芬法建立ICR小鼠子宫腺肌病模型造模率为100%,B组小鼠子宫肌层微血管密度高于A、C组,差异有统计学意义(P<0.05)。②种植窗期子宫内膜LIF蛋白水平A组和C组明显高于B组,差异有统计学意义(P<0.05);A、C组间无统计学差异(P>0.05)。③B组可见较多退化的胞饮突,分布稀疏,呈局灶性分布;A组的胞饮突较B组丰富但大小略不均;C组胞饮突分布较丰富且发育完全。结论:新生小鼠口服他莫西芬法可高效建立子宫腺肌病模型,GnRHa降调节能改善子宫腺肌病小鼠子宫内膜中LIF表达及胞饮突发育,从而提高子宫内膜容受性。
Objective: To investigate the effect of gonadotropin-releasing hormone agonist (GnRHa) on endometrial receptivity in implanted window of adenomyosis model mice. Methods: Neonatal ICR mice were fed with tamoxifen to establish adenomyosis model and were randomly divided into GnRHa model group (A group), model control group (B group), and the same age normal mice as The control group (C group), 8 rats in each group, were sacrificed at 100-115 days of age and the pathological changes of the uterus were detected by HE staining. The density of uterine microvessels was calculated by immunohistochemical staining of CD31. Endometrial LIF expression and scanning electron microscopy observation of the development of pinopodes. Results: ① The rate of myometrial microvessel density in group B was higher than that in group A and C (P <0.05) ). ② The level of LIF protein in the implantation window was significantly higher in group A and group C than in group B (P <0.05). There was no significant difference between group A and C (P> 0.05). ③ In Group B, more degenerated pinopodes were observed, with sparse distribution and focal distribution; Group A had more abundant pinopodes than Group B, but slightly uneven in size; Group C had more abundant and fully developed pinopodes. Conclusion: Newborn mice can be treated with oral tamoxifen to establish a model of adenomyosis. Downregulation of GnRHa can improve the expression of LIF in endometrium of mice with adenomyosis and promote the development of endometriosis. By sexual.