發(fā)布時間：2018-06-17 05:06

  本文選題：解偶聯(lián)蛋白2 + 女性生殖　； 參考：《第一軍醫(yī)大學》2005年博士論文

【摘要】：人類已經(jīng)認識到人類卵母細胞的年齡相關改變與氧化應激有關,抗氧化治療可以部分改善小鼠卵母細胞的年齡相關改變。90年代人們發(fā)現(xiàn)卵泡液活性氧(reactive oxygen species,ROS)水平與體外授精(in-vitro fertilization,IVF)結(jié)局相關,過高的ROS水平提示了不良的IVF結(jié)局。研究還發(fā)現(xiàn)體外培養(yǎng)中過氧化氫可以誘導早期胚胎凋亡。這些結(jié)果提示了氧化還原過程參與生殖過程調(diào)節(jié),生殖細胞和早期胚胎細胞膜富含不飽和脂肪酸,對氧化應激損傷非常敏感,目前的研究多集中于氧化損傷對人類生殖影響方面,對于其生理情況下抗氧化機制少有研究。 解偶聯(lián)蛋白2(uncoupling protein 2,UCP2)是近年發(fā)現(xiàn)的UCPs成員,分子量為33.218kDa,廣泛表達于哺乳動物多種組織,成年Ucp2(-/-)小鼠表型分析顯示UCP2基因與ROS產(chǎn)生調(diào)節(jié)強相關,UCP2通過部分氧化磷酸化解偶聯(lián),降低線粒體膜電位,控制細胞內(nèi)ROS產(chǎn)生,廣泛參與多種組織的抗氧化應激損傷。UCP2的高表達可以增加細胞的抗氧化損傷能力和抑制氧化誘導的細胞凋亡,而UCP2的缺乏導致細胞抗氧化能力下降,組織損傷后修復能力下降。那么人類生殖系統(tǒng)是否存在UCP2表達?UCP2-ROS調(diào)節(jié)系統(tǒng)是人類女性生殖過程中的主要氧化還原調(diào)節(jié)機制嗎?本研究擬在動物研究和人類其它組織研究的基礎上觀察人類女性生殖系統(tǒng)是否存在UCP2的表達及其與卵母細胞和早期胚胎發(fā)育的關系,并探討UCP2參與卵母細胞發(fā)育過程中氧化還原調(diào)節(jié)的機制。
[Abstract]:Humans have recognized that age-related changes in human oocytes are associated with oxidative stress, Antioxidant therapy could partially improve the age-related changes of mouse oocytes. In 1990s, it was found that reactive oxygen species (Ros) level in follicular fluid was associated with the outcome of IVF in vitro insemination. The high Ros level suggested a poor outcome of IVF. It was also found that hydrogen peroxide could induce early embryo apoptosis in vitro. These results suggest that the redox process is involved in the regulation of reproductive process. The germ cells and early embryonic cell membranes are rich in unsaturated fatty acids and are sensitive to oxidative stress damage. Most of the current studies focus on the effects of oxidative damage on human reproduction, and few studies have been conducted on the antioxidant mechanism under physiological conditions. Uncoupling protein (2(uncoupling protein 2) is a member of UCPs (molecular weight 33.218 kDa), which is widely expressed in many mammalian tissues. Phenotype analysis of adult UCP2 / UCP2 / UCP2 mice shows that UCP2 gene is strongly related to Ros production and the coupling is mediated by partial oxidative phosphoric acid. Decreasing mitochondrial membrane potential, controlling the production of Ros in cells, and participating in the high expression of antioxidant stress injury. UCP2 can increase the ability of antioxidant injury and inhibit the apoptosis induced by oxidation. But the deficiency of UCP2 resulted in the decrease of cell antioxidant ability and the decrease of repair ability after tissue injury. So is there a UCP2 expression UCP2-ROS regulatory system in the human reproductive system that is the main redox regulatory mechanism in the human female reproductive process? This study aims to investigate the expression of UCP2 in human female reproductive system and its relationship with oocyte and early embryonic development based on animal studies and other human tissue studies. The mechanism of UCP2 involved in redox regulation during oocyte development was discussed.
【學位授予單位】：第一軍醫(yī)大學
【學位級別】：博士
【學位授予年份】：2005
【分類號】：R33

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1 歐健;大黃素對脂肪變性LO2肝細胞UCP2 mRNA表達的影響[D];暨南大學;2009年

2 梁彥超;慢性阻塞性肺疾病患者肺組織中PRMT6的表達及意義[D];中南大學;2013年

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本文編號：2029845