UCP2在女性生殖中作用的研究

发布时间：2018-06-17 05:06

本文选题：解偶联蛋白2 + 女性生殖　；参考：《第一军医大学》2005年博士论文

【摘要】：人类已经认识到人类卵母细胞的年龄相关改变与氧化应激有关,抗氧化治疗可以部分改善小鼠卵母细胞的年龄相关改变。90年代人们发现卵泡液活性氧(reactive oxygen species,ROS)水平与体外授精(in-vitro fertilization,IVF)结局相关,过高的ROS水平提示了不良的IVF结局。研究还发现体外培养中过氧化氢可以诱导早期胚胎凋亡。这些结果提示了氧化还原过程参与生殖过程调节,生殖细胞和早期胚胎细胞膜富含不饱和脂肪酸,对氧化应激损伤非常敏感,目前的研究多集中于氧化损伤对人类生殖影响方面,对于其生理情况下抗氧化机制少有研究。解偶联蛋白2(uncoupling protein 2,UCP2)是近年发现的UCPs成员,分子量为33.218kDa,广泛表达于哺乳动物多种组织,成年Ucp2(-/-)小鼠表型分析显示UCP2基因与ROS产生调节强相关,UCP2通过部分氧化磷酸化解偶联,降低线粒体膜电位,控制细胞内ROS产生,广泛参与多种组织的抗氧化应激损伤。UCP2的高表达可以增加细胞的抗氧化损伤能力和抑制氧化诱导的细胞凋亡,而UCP2的缺乏导致细胞抗氧化能力下降,组织损伤后修复能力下降。那么人类生殖系统是否存在UCP2表达?UCP2-ROS调节系统是人类女性生殖过程中的主要氧化还原调节机制吗?本研究拟在动物研究和人类其它组织研究的基础上观察人类女性生殖系统是否存在UCP2的表达及其与卵母细胞和早期胚胎发育的关系,并探讨UCP2参与卵母细胞发育过程中氧化还原调节的机制。
[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.
【学位授予单位】：第一军医大学
【学位级别】：博士
【学位授予年份】：2005
【分类号】：R33

【共引文献】