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Co-Enzyme Q10 Supplementation Rescues Cumulus Cells Dysfunction in a Maternal Aging Model

机译:辅酶Q10补充可挽救孕产妇衰老模型中的积木细胞功能障碍

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摘要

Over the past four decades, due to cultural and social changes, women in the developed world have significantly delayed childbirth. This trend is even worse for patients who attend infertility clinics. It is well-known that live birth rates in women older than 35 are significantly lower than in those younger, both naturally and with assisted reproduction. Fertility decline is, in part, due to an increase in oocyte aneuploidy that leads to a reduced embryo quality, as well as an increased incidence of miscarriages and birth defects. Here we show that aging-associated malfunction is not restricted to the oocyte, as cumulus granulosa cells also display a series of defects linked to mitochondrial activity. In, both, human and mouse model, a decline in cumulus cell function due to increased maternal age is accompanied by a decreased expression of enzymes responsible for Coenzyme Q (CoQ) production, particularly Pdss2 and CoQ6. In an aged mouse model supplementation with Coenzyme Q10—a potent stimulator of mitochondrial function—restored cumulus cell number, stimulated glucose uptake, and increased progesterone production. CoQ10 supplementation might, thus, improve oocyte and cumulus cells quantity and quality, by improving the mitochondrial metabolism in females of advanced maternal age.
机译:在过去的四十年中,由于文化和社会的变化,发达国家的妇女大大延迟了分娩。对于去不孕诊所的患者来说,这种趋势更加严重。众所周知,自然和有辅助生殖的35岁以上妇女的活产率明显低于年轻妇女。生育能力下降部分是由于卵母细胞非整倍性增加导致胚胎质量下降,以及流产和出生缺陷的发生率增加。在这里,我们显示与衰老相关的功能异常不仅限于卵母细胞,因为卵丘颗粒细胞还显示出与线粒体活性相关的一系列缺陷。在人类和小鼠模型中,由于产妇年龄增加导致的卵丘细胞功能下降伴随着负责辅酶Q(CoQ)产生的酶,特别是Pdss2和CoQ6的表达降低。在老年小鼠模型中补充辅酶Q10(一种有效的线粒体功能刺激剂)可以恢复卵丘细胞数,刺激葡萄糖摄取和增加孕激素生成。因此,辅酶Q10的补充可能会通过改善孕妇高龄女性的线粒体代谢,从而改善卵母细胞和卵丘细胞的数量和质量。

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