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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/23169
Title: | Lcn2蛋白活化巨噬細胞與子宮內膜異位症之相關研究 Study of the relationship between Lcn2 protein-activated macrophage and endometriosis |
Authors: | Che-Yu Lin 林哲宇 |
Advisor: | 朱善德(Sin-Tak Chu) |
Keyword: | 巨噬細胞,疏水性結合蛋白,子宮內膜異位, Lcn2,macrophage,endometriosis, |
Publication Year : | 2009 |
Degree: | 碩士 |
Abstract: | Lcn2蛋白屬於疏水性分子結合蛋白家族中的一員,為急性期反應蛋白之一,實驗室先前研究指出小鼠子宮Lcn2蛋白可以透過小鼠動情週期之類固醇荷爾蒙調控,以Lcn2蛋白處理人類子宮內膜細胞株(RL95-2)會刺激IL-8和MCP-1的表現,同時使細胞凋亡停止。子宮內膜異位症是由雌激素刺激子宮內膜細胞過度增生所發生的疾病,而IL-8和MCP-1會參與誘導子宮內膜異位症的形成。為了瞭解Lcn2是否於子宮內膜異位症形成過程中可能參與的生理功能,利用手術建立小鼠子宮內膜異位症的模式以及純化自小鼠子宮分泌液中的Lcn2蛋白對小鼠巨噬細胞進行研究,以瞭解Lcn2蛋白在子宮內膜異位症中經由巨噬細胞所參與的可能分子機制。實驗中發現子宮內膜異位症的小鼠腹腔液中Lcn2濃度較高。此外實驗證實Lcn2於無血清狀態測定巨噬細胞活化因子iNOS、TNF-α均顯示巨噬細胞是Lcn2刺激而活化,同時會使活化的巨噬細胞產生IL-6、GCSF、RANTES、COX-2、MIP-2、MCP-1等與子宮內膜異位症形成相關的因子。推測高濃度的Lcn2在腹腔液中可活化巨噬細胞與誘導子宮內膜異位症的形成可能有密切的關係。 Lcn2 protein, a lipocalin, is one of the acute phase proteins. According to our previous data, ovarian steroids regulate the expression of Lcn2 during the estrous cycle. Besides, Lcn2 protein has been found to induce IL-8 and MCP-1 expression in human endometrial carcinoma cell line (RL95-2). There are substantial evidences showing that the progression of endometriosis is estrogen-dependent and that increased levels of cytokines such as IL-8 and MCP-1 are associated with endometriosis formation. In this study, a mouse model of surgically induced endometriosis and a mouse macrophage cell line (RAW264.7) were used to investigate the role of Lcn2 during the development of endometriosis. We demonstrated that during endometriosis formation, the levels of Lcn2 were increased in the peritoneal fluid. Treatment of RAW264.7 cells with Lcn2 resulted in the activation of macrophages. This was accompanied by the elevation of iNOS and TNF-α and the secretion of cytokines, including IL-6, GCSF, RANTES, COX-2, MIP-2 and MCP-1, all of which are factors that facilitate the development of endometriosis. In conclusion, Lcn2 may trigger the activation of macrophages in the peritoneal fluid and thus promote the development of endometriosis. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/23169 |
Fulltext Rights: | 未授權 |
Appears in Collections: | 生化科學研究所 |
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ntu-98-1.pdf Restricted Access | 1.35 MB | Adobe PDF |
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