發(fā)布時間：2018-02-01 11:33

  本文關鍵詞： 子癇前期 AMPK HTR8/SVneo 代謝組學　出處：《重慶醫(yī)科大學》2017年碩士論文　論文類型：學位論文

【摘要】：背景:子癇前期(Preeclampsia,PE)是一種常見的妊娠期特有疾病,是引起母胎發(fā)病和死亡的重要原因,其發(fā)病原因和機制研究甚多,但不明確,可能涉及胎盤、胎兒和母體多方面因素。研究顯示絨毛外滋養(yǎng)細胞侵襲不足,子宮螺旋動脈重鑄障礙,導致胎盤缺血缺氧是子癇前期重要的病理特征,因此子癇前期又被稱為是胎盤缺血性疾病。AMPK是生物能量代謝調節(jié)的關鍵分子,在多種代謝性疾病中通過調節(jié)葡萄糖攝取和脂肪酸代謝發(fā)揮重要作用。因此我們通過研究子癇前期代謝組學變化,檢測相關代謝通路生物分子變化探究子癇前期的病理機制,為臨床預測及治療提供依據。方法:收集正常孕婦及子癇前期孕婦胎盤組織,建立細胞模型,GC-MS進行代謝組學分析,q-PCR和Western Blotting檢測相關基因及蛋白表達;MDA檢測脂質氧化水平;ACEA實時細胞計數(shù)儀及transwell檢測滋養(yǎng)細胞的遷移侵襲能力。結果:子癇前期孕婦胎盤組織代謝組學發(fā)生改變(p0.05),AMPK磷酸化水平明顯升高(N=16,p0.05);成功建立子癇前期體外細胞模型,缺氧上調滋養(yǎng)細胞AMPK表達(N=6,p0.05),抑制滋養(yǎng)細胞遷移侵襲能力,改變滋養(yǎng)細胞的代謝組學。結論:子癇前期孕婦代謝失衡;缺氧時滋養(yǎng)細胞優(yōu)先利用短鏈脂肪酸;缺氧激活AMPK進而抑制滋養(yǎng)細胞的遷移侵襲能力。
[Abstract]:Background: Preeclampsiaena preeclampsis (PEI) is a common gestational disease and an important cause of maternal and fetal morbidity and mortality. The etiology and mechanism of preeclampsis preeclampsis (PEP) is much studied, but it is not clear and may involve placenta. Fetal and maternal factors. Studies have shown that inadequate invasion of extravillous trophoblast and dysplasia of uterine spiral artery lead to placental ischemia and hypoxia as an important pathological feature of preeclampsia. Therefore, preeclampsia is also called placental ischemic disease. AMPK is a key molecule in the regulation of biological energy metabolism. It plays an important role in many metabolic diseases by regulating glucose uptake and fatty acid metabolism. Therefore, we explore the pathological mechanism of preeclampsia by studying the changes of preeclampsia metabolomics and detecting the biomolecular changes of related metabolic pathways. Methods: the placental tissues of normal and preeclampsia pregnant women were collected. In order to establish a cell model, GC-MS was used to detect the expression of related genes and proteins by Western Blotting. ACEA real-time cell counter and transwell were used to detect the migration and invasion ability of trophoblastic cells in preeclampsia. The changes of placental tissue metabolism in pregnant women showed that the level of AMPK phosphorylation in placenta of pregnant women was significantly increased, and the in vitro cell model of preeclampsia was successfully established. Hypoxia upregulated the expression of AMPK in trophoblast, inhibited the migration and invasion of trophoblast and changed the metabolism of trophoblast. Conclusion: the metabolic imbalance of preeclampsia pregnant women, trophoblast preterm preeclampsia preferentially uses short chain fatty acid. Hypoxia activates AMPK and inhibits trophoblast migration and invasion.
【學位授予單位】：重慶醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R714.244

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