本文關(guān)鍵詞： 子癇前期 AMPK HTR8/SVneo 代謝組學(xué)　出處：《重慶醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)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(jī)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(xì)胞侵襲不足,子宮螺旋動(dòng)脈重鑄障礙,導(dǎo)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(diào)節(jié)的關(guān)鍵分子,在多種代謝性疾病中通過調(diào)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(xué)變化,檢測(cè)相關(guān)代謝通路生物分子變化探究子癇前期的病理機(jī)制,為臨床預(yù)測(cè)及治療提供依據(jù)。方法:收集正常孕婦及子癇前期孕婦胎盤組織,建立細(xì)胞模型,GC-MS進(jìn)行代謝組學(xué)分析,q-PCR和Western Blotting檢測(cè)相關(guān)基因及蛋白表達(dá);MDA檢測(cè)脂質(zhì)氧化水平;ACEA實(shí)時(shí)細(xì)胞計(jì)數(shù)儀及transwell檢測(cè)滋養(yǎng)細(xì)胞的遷移侵襲能力。結(jié)果:子癇前期孕婦胎盤組織代謝組學(xué)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(xì)胞模型,缺氧上調(diào)滋養(yǎng)細(xì)胞AMPK表達(dá)(N=6,p0.05),抑制滋養(yǎng)細(xì)胞遷移侵襲能力,改變滋養(yǎng)細(xì)胞的代謝組學(xué)。結(jié)論:子癇前期孕婦代謝失衡;缺氧時(shí)滋養(yǎng)細(xì)胞優(yōu)先利用短鏈脂肪酸;缺氧激活A(yù)MPK進(jìn)而抑制滋養(yǎng)細(xì)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(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R714.244

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