發(fā)布時間：2018-04-23 11:44

  本文選題：脂氧素 + 子宮內(nèi)膜異位癥��； 參考：《廈門大學(xué)》2014年碩士論文

【摘要】：目的：研究脂氧素A4(lipoxin A,LXA4)與雌激素受體(estrogen receptor,ER)、孕激素受體(progestrone receptor, PR)之間的關(guān)系,探索LXA4對ER、PR表達(dá)的影響及LXA4對ER-p38絲裂原活化蛋白激酶(p38mitogen-activated protein kinase, p38MAPK)串話通路的調(diào)節(jié)作用。 方法：采用酶聯(lián)免疫吸附試驗、實時熒光定量PCR和免疫組織化學(xué)法檢測內(nèi)異癥患者及正常婦女中LXA、ER、PR的表達(dá)。通過實時熒光定量PCR檢測ER、PR、腫瘤壞死因子-a(tumor necrosis factor-alpha, TNF-a)、白介素-6(interleukin-6,IL-6)的mRNA表達(dá)。利用western blot和免疫組織化學(xué)法檢測p38MAPK的磷酸化。采用熒光素酶報告基因測定雌激素反應(yīng)元件(estrogen response element, ERE)的轉(zhuǎn)錄活性。利用MTS法和EdU法檢測LXA4對子宮內(nèi)膜異位間質(zhì)細(xì)胞(endometriotic stromal cells, ESCs)增殖的影響。 結(jié)果：在正常子宮內(nèi)膜組織中,ERa和ERβmRNA均存在周期性變化規(guī)律,而在異位病灶中,ERa和ERβmRNA在不同月經(jīng)周期中的表達(dá)情況無明顯改變,失去周期性變化規(guī)律。LXA、ERa和PR在內(nèi)異癥患者病灶組織中低表達(dá),ERβ在異位病灶組織中顯著高表達(dá)。外源性LXA4可以明顯上調(diào)ERβ的表達(dá),而ERp特異性激動劑DPN可以抑制p38MAPK磷酸化。同時LXA4可以抑制雌二醇(estradiol,E2)誘導(dǎo)的p38MAPK的磷酸化及其下游細(xì)胞炎性因子TNF-a和IL-6的表達(dá),抑制E2誘導(dǎo)的ESCs的增殖。 結(jié)論：LXA4可以促進(jìn)ESCs中ERβ的表達(dá),并很可能通過ERβ抑制E2誘導(dǎo)的p38MAPK磷酸化,從而抑制異位病灶的生長。
[Abstract]:Aim: to investigate the relationship between lipoxygenin A4(lipoxin Agna _ 4 and estrogen receptor estrogen receptor ERA, progesterone receptor progestrone receptor, and to explore the effect of LXA4 on ERP PR expression and the regulation of LXA4 on ER-p38 mitogen-activated protein kinase (p38MAPK) crosstalk pathway. Methods: enzyme linked immunosorbent assay (Elisa), real-time fluorescence quantitative PCR and immunohistochemistry were used to detect the expression of LXA ERP PR in patients with endometriosis and normal women. The mRNA expression of ERP, tumor necrosis factor-alpha, TNF-a, interleukin-6 interleukin-6 (IL-6) was detected by real-time fluorescence quantitative PCR. Western blot and immunohistochemistry were used to detect the phosphorylation of p38MAPK. The transcriptional activity of estrogen response element (ERE) was determined by luciferase reporter gene. The effects of LXA4 on the proliferation of endometrial stromal stromal cells (ESCs) were detected by MTS and EdU. Results: in normal endometrium, there were periodic changes of ERa and ER 尾 mRNA, but there was no significant change in the expression of ERa and ER 尾 mRNA in ectopic lesions in different menstrual cycles. The expression of ER 尾 was significantly higher in ectopic lesions than that in patients with LXA ERa and PR. Exogenous LXA4 could significantly up-regulate the expression of ER 尾, while ERp specific agonist DPN could inhibit p38MAPK phosphorylation. At the same time, LXA4 could inhibit the phosphorylation of p38MAPK induced by estradiolium E _ 2 and the expression of TNF-a and IL-6, as well as the proliferation of ESCs induced by E _ 2. Conclusion: the expression of ER 尾 in ESCs can be promoted by WLXA4, and it is possible that ER 尾 inhibits the p38MAPK phosphorylation induced by E2 and thus inhibits the growth of ectopic lesions.
【學(xué)位授予單位】：廈門大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R711.71

【參考文獻(xiàn)】

相關(guān)期刊論文 前5條

1 郎景和;;關(guān)于子宮內(nèi)膜異位癥的再認(rèn)識及其意義[J];中國工程科學(xué);2009年10期

2 鄭娟;祁曉晨;崔毓桂;;局部高雌激素與子宮內(nèi)膜異位癥[J];國際生殖健康/計劃生育雜志;2013年02期

3 陳瓊?cè)A,曲軍英,邱娜璇,許雅云,高凌云,鄭偉;MMP9、TIMP1及VEGF在子宮內(nèi)膜異位癥患者在位內(nèi)膜的表達(dá)[J];基礎(chǔ)醫(yī)學(xué)與臨床;2004年04期

4 陳瓊?cè)A;邱娜璇;濮德敏;周玉明;李天;楊宏毅;;Change Profiles in Matrix Metalloproteinase-2 and-9 in Induced Endometriosis in Mice[J];Journal of Huazhong University of Science and Technology(Medical Sciences);2010年02期

5 陽艷軍;冷金花;董U，

本文編號：1791832