透明带3多肽诱导的免疫性卵巢早衰小鼠模型子宫组织中Ki-67、ER的表达  

Expression of Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure induced by peptide zona pellucida 3

作　　者：蔡慧华[1] 付霞霏[1] 任旭雯 陈夏珠[1] 张冬梅[1] 何援利[1] 

机构地区：[1]南方医科大学珠江医院妇产科,广东广州510280

出　　处：《南方医科大学学报》2015年第7期992-997,共6页Journal of Southern Medical University

基　　金：广州市科技计划项目(11C32120702);广东省科技计划项目(2012B031800123);广东高校优秀青年创新人才培养计划项目育苗工程(2012LYM_0034)

摘　　要：目的：以透明带3多肽（pZP3）诱导的免疫性卵巢早衰（POF）小鼠为研究对象，观察其子宫Ki-67、雌激素受体（ER）的表达，以进一步探讨免疫性卵巢早衰患者辅助生殖相关的子宫预处理方案。方法取7~8周龄的健康雌性BALB/c小鼠40只，随机分为对照组和模型组。通过阴道脱落细胞涂片、血清性激素、卵巢组织形态及抗卵巢ZP3抗体鉴定建模成功。检测两组小鼠子宫组织形态变化及子宫Ki-67、雌激素受体α亚型（ERα）及雌激素受体β亚型（ERβ）的表达。结果8周后80%小鼠建模成功。与对照组相比，模型组子宫萎缩，内膜变薄，单位面积内腺体数量减少。模型组子宫内膜上皮细胞、腺上皮细胞及间质细胞中Ki-67的表达较对照组减弱，且有胞核转位至胞浆现象。对照组小鼠子宫内膜上皮细胞、腺上皮细胞及间质细胞的胞浆强表达ERα，而模型组呈阴性表达。两组小鼠子宫内膜ERβ均呈阴性表达。结论 pZP3可以诱导小鼠成功构建免疫性卵巢早衰疾病模型，同时引起子宫内膜上皮细胞及间质细胞的增殖降低和ERα表达减弱。Objective To investigate the histomorphology and the expressions of the proliferation marker Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure （POF） induced by zona pellucida 3 peptide （pZP3）. Methods Autoimmune POP models were established in 20 female BALB/c mice （7-8 weeks old） by immunization with pZP3 and another 20 mice served as the control group. The POP models were verified by vaginal cytology, serum sex hormones, ovary histomorphology and ZP3 antibody immunohistochemistry. The histomorphology and expressions of Ki-67, estrogen receptorαand estrogen receptorβin the uterus of the mice were detected. Results Autoimmune POP models were estblished successfully in 80%of the mice at 8 weeks after the immunization. Compared with those in the control group, the mice in the model group showed a smaller volume of the uterus, thinner endometrium and a reduced number of glands. The luminal epithelial cells, glandular epithelial cells and stromal cells in the uterus of the model mice all presented with a lower expression of Ki-67 than those in the control group, and Ki-67 translocation from the nuclei to the cytoplasm was found in the model group. The luminal epithelial cells, glandular epithelial cells and stromal cells showed positive ERαimmunoreactivity in the model group but not in the control group. No obvious ERβexpression was found in the uterus in either of the groups. Conclusion pZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERαin the uterus of mice.

关 键 词：免疫性卵巢早衰 透明带3多肽 子宫内膜 KI-67 雌二醇 

分 类 号：R711.75[医药卫生—妇产科学] R-332[医药卫生—临床医学]