国际妇产科学杂志
國際婦產科學雜誌
국제부산과학잡지
Journal Of International Obstetrics And Gynecology
2015年
5期
500-503
,共4页
雍敏婕%李文倩%王芳%金伟%刘波%于晓辉
雍敏婕%李文倩%王芳%金偉%劉波%于曉輝
옹민첩%리문천%왕방%금위%류파%우효휘
受体,雌激素%受体,trkB%子宫内膜异位症%子宫内膜
受體,雌激素%受體,trkB%子宮內膜異位癥%子宮內膜
수체,자격소%수체,trkB%자궁내막이위증%자궁내막
Receptors,estrogen%Receptor,trkB%Endometriosis%Endometrium
目的：检测雌激素受体（ER）和酪氨酸激酶受体B（TrkB）在子宫内膜异位症（EMs）患者在位和异位内膜组织中的表达，评价ER和TrkB在EMs发病中的作用。方法：选择18例卵巢EMs病例，其中在位内膜增殖期9例、分泌期9例。采用实时聚合酶链反应（real time PCR）、蛋白质印迹法（Western blotting）和免疫组织化学法检测ERα、ERβ、TrkB和脑源性神经营养因子（BDNF）mRNA和蛋白质的表达。结果：EMs患者在位内膜ERαmRNA和蛋白表达高于异位内膜组织，而ERβ、TrkB mRNA和蛋白的表达均低于异位内膜组织，差异有统计学意义（均P＜0.05）。异位内膜组织中ERβ/ERαmRNA的比值高于在位内膜组。在EMs在位内膜中，ERα、ERβ、TrkB蛋白的表达在增殖期均高于分泌期（均P＜0.05）。 ERα主要表达于在位内膜细胞核内；ERβ主要表达于异位内膜细胞质中；ERα与ERβ在EMs在位内膜的增殖期着色比分泌期更加明显。 EMs的在位内膜和异位内膜组织中TrkB与BDNF都有表达，且主要集中于细胞质。 EMs在位内膜中TrkB蛋白质在增殖期表达更明显。结论：ERβ和TrkB可能在EMs的发病机制中发挥作用。
目的：檢測雌激素受體（ER）和酪氨痠激酶受體B（TrkB）在子宮內膜異位癥（EMs）患者在位和異位內膜組織中的錶達，評價ER和TrkB在EMs髮病中的作用。方法：選擇18例卵巢EMs病例，其中在位內膜增殖期9例、分泌期9例。採用實時聚閤酶鏈反應（real time PCR）、蛋白質印跡法（Western blotting）和免疫組織化學法檢測ERα、ERβ、TrkB和腦源性神經營養因子（BDNF）mRNA和蛋白質的錶達。結果：EMs患者在位內膜ERαmRNA和蛋白錶達高于異位內膜組織，而ERβ、TrkB mRNA和蛋白的錶達均低于異位內膜組織，差異有統計學意義（均P＜0.05）。異位內膜組織中ERβ/ERαmRNA的比值高于在位內膜組。在EMs在位內膜中，ERα、ERβ、TrkB蛋白的錶達在增殖期均高于分泌期（均P＜0.05）。 ERα主要錶達于在位內膜細胞覈內；ERβ主要錶達于異位內膜細胞質中；ERα與ERβ在EMs在位內膜的增殖期著色比分泌期更加明顯。 EMs的在位內膜和異位內膜組織中TrkB與BDNF都有錶達，且主要集中于細胞質。 EMs在位內膜中TrkB蛋白質在增殖期錶達更明顯。結論：ERβ和TrkB可能在EMs的髮病機製中髮揮作用。
목적：검측자격소수체（ER）화락안산격매수체B（TrkB）재자궁내막이위증（EMs）환자재위화이위내막조직중적표체，평개ER화TrkB재EMs발병중적작용。방법：선택18례란소EMs병례，기중재위내막증식기9례、분비기9례。채용실시취합매련반응（real time PCR）、단백질인적법（Western blotting）화면역조직화학법검측ERα、ERβ、TrkB화뇌원성신경영양인자（BDNF）mRNA화단백질적표체。결과：EMs환자재위내막ERαmRNA화단백표체고우이위내막조직，이ERβ、TrkB mRNA화단백적표체균저우이위내막조직，차이유통계학의의（균P＜0.05）。이위내막조직중ERβ/ERαmRNA적비치고우재위내막조。재EMs재위내막중，ERα、ERβ、TrkB단백적표체재증식기균고우분비기（균P＜0.05）。 ERα주요표체우재위내막세포핵내；ERβ주요표체우이위내막세포질중；ERα여ERβ재EMs재위내막적증식기착색비분비기경가명현。 EMs적재위내막화이위내막조직중TrkB여BDNF도유표체，차주요집중우세포질。 EMs재위내막중TrkB단백질재증식기표체경명현。결론：ERβ화TrkB가능재EMs적발병궤제중발휘작용。
Objective:To detect the expression of estrogen receptor (ER) and TrkB in eutopic endometrium and ectopic endometrium in patients with endometriosis, and explore the potential effect of ER and TrkB in the pathogenesis of EMs. Methods:The expressions of ERα, ERβ, TrkB and BDNF in 18 cases with EMs (include 9 proliferating phase cases and 9 secretory phase of eutopic endometrium) were examined using real-time PCR, Western blotting and immunohistochemistry. Results:At mRNA and protein levels, the expression of ERαin eutopic endometrium was higher than ectopic endometrium with endometriosis, while the expression of ERβ and TrkB in eutopic endometrium were lower than ectopic endometrium with endometriosis, all of that difference have statistically significant (P<0.05). Higher ratio of ERβ/ERαmRNA was found in ectopic endometriosis than eutopic endometrium. In eutopic endometrium, ERα, ERβ and TrkB proteins were mainly expressed in proliferative phase than that in secretory phase (P<0.05). ERα expression was mainly found in cell nucleus of eutopic endometrium, while ERβwas mainly found in cytoplasm of ectopic endometrium. The expression of ERαand ERβwere more obvious in EMs eutopic endometrium proliferative phase than that in secretory phase. TrkB and BDNF were expressed in both eutopic and ectopic endometrium with EMs, and were mainly expressed in cytoplasm. TrkB was more obvious in proliferative phase eutopic endometrium of EMs. Conclusions:ERβand TrkB may mediate the pathogenesy of EMs.
