女性賀爾蒙接受器α及β和超氧歧化酵素在人類子宮內膜異位症表現之研究; Studies on the Expression of Estrogen Receptor-αand —β and Superoxide Dismutase in Human Endometriosis

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Title:	女性賀爾蒙接受器α及β和超氧歧化酵素在人類子宮內膜異位症表現之研究;Studies on the Expression of Estrogen Receptor-αand —β and Superoxide Dismutase in Human Endometriosis
Authors:	林武周;Wu-Chou Lin
Contributors:	中國醫藥學院醫學研究所
Keywords:	女性賀爾蒙接受器α;女性賀爾蒙接受器β;超氧歧化酵素;子宮內膜異位症;Estrogen Receptor-α;Estrogen Receptor-β;Superoxide Dismutase;Endometriosis
Date:	1999
Issue Date:	2009-12-02 14:11:56 (UTC+8)
Abstract:	子宮內膜異位症是一種慢性、持續性且易復發的婦科疾病，經常伴隨有經痛及不孕的問題，影響著許多婦女的情緒壓力及身心健康。它雖然是為良性的疾病，確有著類似癌症的病理特性，如沾粘、侵犯和轉移，其病理機制至今未明，也尚無根治的方法，這有待作更進一步的研究來解決之。子宮內膜異位症的臨床表現與女性賀爾蒙的存在與否有極大的關係。在子宮內膜異位瘤的基質底部，可見明顯的發炎反應、炎症細胞聚集、局部的細胞激素和超氧自由基分泌等現象，所以在「實驗一」中觀察女性賀爾蒙接受器（estrogen receptor；ER）家族中a及b兩種亞型的表現，探討在不同亞型的ER與子宮內膜異位症的相關性。在「實驗二」中則觀察銅鋅超氧岐化物（Cu,Zn-SOD）表現，探討超氧自由基與其病理機制間之關連性。選擇25-35歲月經年齡之子宮內膜異位症患者，其手術取出之卵巢子宮內膜異位瘤及其子宮內膜作為實驗組；對照組為子宮頸原位癌患者在椎狀切除手術中取出之子宮內膜。利用RT-PCR、免疫化學組織染色及西方點墨法來觀察mRNA及蛋白質表現。結果發現在子宮內膜異位瘤中，其ER-a之蛋白及mRNA表現較子宮內膜異位者減少，而ER-b蛋白及mRNA表現則增強。可能意味著子宮內膜異位細胞之ER-a有缺損，雖然ER-b表現增加，但不能完全代償ER-a之功能。此變化可能與其臨床病理表現有著重要關連性。在「實驗二」中Cu,Zn-SOD只在子宮內膜異位瘤基質的底部才有明顯表現，在此同時也可觀察到ER-a、b的表現，尤其ER-a較為明顯，而正好是子宮內膜異位瘤所侵犯破壞其鄰近組織的地方。我們的推論ER-a、b與Cu,Zn-SOD間相互具有調控功能，在子宮內膜異位細胞的病理機制中可能扮演著協同的調控角色。這些需要更進一步的實驗來證實。; Endometriosis, the chronic Gyn. disease with high relapse rate, presented the symptoms and signs of dysmenorrhea and infertility. It was a benign disease but with cancer-like behavior including adhesions, invasion and metastasis. There were no causal therapy due to unclear pathogenesis till now. Owing to estrogen-dependent characteristics, we choused estrogen receptor-a and -b isoforms and Cu,Zn-SOD expression in endometrium and endometrioma of reproductive women. Main outcome were measured with RT-PCR for ER-a and -b mRNA, IHC and Western blot for ER-a, -b and Cu,Zn-SOD protein expressions. The results revealed that the ER-a mRNA and protein were lower in endometrioma than in endometrium, but ER-b mRNA and protein higher. ER--a and -b showed some expression in stroma of endometroma. Cu,Zn-SOD expressed markly in deep stroma of endometrioma. It might be concluded that ER-a might be damaged in ovarian endometrioma, and ER-b might fail to act with ER-a for normal estrogen dependency. This endocrinological status might lead to unigue estrogen-dependent growth, invasion and spreading of endometrioma, but need further studies to see the its real pathogenesis.
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