FKBP52、PR、MMP-2和ER在小鼠腺肌症子宫内膜组织中的表达和意义

Expression and significant of FKBP52,PR,MMP2 and ER in endometrium of mice with adenomyosis

目的:观察FK506结合蛋白52(FKBP52)、孕激素受体(PR)、基质金属蛋白酶-2(MMP-2)和雌激素受体(ER)在子宫内膜腺肌症模型小鼠子宫内膜中的表达,为探讨其在子宫内膜腺肌症中的作用提供依据。方法:采用化学诱导法构建小鼠腺肌症模型,从小鼠出生第2天开始分别给予0.6,3mg/kg托瑞米芬灌胃(共2组),同时设立对照组,每组15只新出生雌鼠。常规喂养小鼠至5个月,免疫组织化学检测小鼠子宫内膜组织FKBP52、PR、MMP-2和ER蛋白的定位及表达,采用Realtime-RT-PCR检测FKBP52、PR、MMP-2和ER的表达。结果:托瑞米芬诱导新生小鼠腺肌症模型成功,FKBP52、PR在腺肌症模型小鼠子宫内膜中的表达低于正常对照小鼠;MMP-2和ER在腺肌症模型小鼠子宫内膜组织中的表达高于正常对照小鼠。结论:FKBP52、PR、ER和MMP-2在腺肌症模型小鼠和正常对照小鼠子宫中的差异表达可能与腺肌症的发生发展有关。

Objective： To investigate the expression of FKBP52, PR, MMP2, and ER in endometrium of mice with adenomyosis, and to explore their roles in the pathogenesis of adenomyosis. Methods： Chemical induction method was used to construct the mice model with adenomyosis. Female mice had given toremifene 0.6 or 3 mg/kg after born 2days through intragastric administration （15 mice in each group）, at the same time, 15 normal female mice were in control group. After all mice sexual maturity, the expression of FKBP52, PR, MMP2, and ER in endometrium of mice with adenomysis or normal mice were detected by immunohistochemistry and real time RT PCR. Results： Torrimifen had induced successful mice model with adenomyosis in newborn mice. The expressions of FKBP52 and PR in endometrium of mice with adenomyosis were significantly lower than those of normal mice, and the expression of MMP 2 and ER in endometrium of mice with adenomyosis were significantly higher than those of normal mice. Conclusion： Mice with or without adenomysosis had different expression of FKBP52, PR, MMP2, and ER in their endometrium, which maybe play important roles in the pathogenesis of adenomyosis.