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首页> 外文期刊>Biopreservation and biobanking >Prematuration Culture with Phosphodiesterase Inhibitors After Vitrification May Induce Recovery of Mitochondrial Activity in Vitrified Mouse Immature Oocytes
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Prematuration Culture with Phosphodiesterase Inhibitors After Vitrification May Induce Recovery of Mitochondrial Activity in Vitrified Mouse Immature Oocytes

机译：在玻璃化后，具有磷酸二酯酶抑制剂的前饱和培养物可诱导玻璃化小鼠未成熟卵母细胞中的线粒体活性恢复

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This study investigates the possible causes for low development of blastocysts in vitrified immature oocytes by evaluating the changes of mitochondrial membrane potential and reactive oxygen species (ROS) production and finds a recovery mechanism for these conditions in vitrified immature oocytes. To recover from the cryoinjury, we cultured vitrified immature oocytes in milrinone containing medium for 1, 3, and 5 hours and then extended the culture for oocyte maturation. There was no difference in in vitro maturation and fertilization rate between fresh and vitrified/warmed oocytes. However, the development rate of blastocysts in vitrified/warmed oocytes was significantly lower than that in fresh oocytes (p0.05). The development rate of blastocysts was recovered if these oocytes were cultured for 3 hours in milrinone. Vitrified/warmed oocytes incubated in milrinone for 0 and 1 hour showed a significantly higher level of ROS (p0.05) and a significantly lower mitochondrial membrane potential (p0.05) than fresh oocytes. However, there was no significant difference (p0.05) between vitrified oocytes incubated in milrinone for 3 hours and fresh oocytes in terms of ROS level and mitochondrial membrane potential. In conclusion, alteration of highly polarized mitochondria distribution in vitrified oocytes may have an effect on mitochondrial activity, including ROS production during fertilization and further development. Preincubation in milrinone before in vitro maturation of immature vitrified/warmed oocytes may help the redistribution of highly polarized mitochondrial inner membrane potential and in reducing ROS and enhance the further embryonic development after fertilization.
机译：本研究通过评估线粒体膜电位和反应性氧物质（ROS）产生的变化，研究了玻璃化未成熟卵母细胞中胚泡低发育的可能原因，并在玻璃化未成熟的卵母细胞中发现这些条件的回收机制。从低温尼康复中恢复，我们培养含有米隆酮培养基的玻璃化未成熟卵母细胞1,3和5小时，然后延长卵母细胞成熟的培养物。新鲜和玻璃化/温热卵母细胞之间的体外成熟和施肥率没有差异。然而，玻璃化/升温卵母细胞中胚泡的发育速率明显低于新鲜卵母细胞（P <0.05）。如果将这些卵母细胞培养3小时，则回收胚泡的开发速率。在MilrinOne中孵育的玻璃化/温热的卵母细胞0和1小时显示出比新鲜卵母细胞显着更高水平的ROS（P <0.05）和显着降低的线粒体膜电位（P <0.05）。然而，在MilRinone温育3小时和新鲜卵母细胞的玻璃化卵母细胞之间没有显着差异（P> 0.05），并且在ROS水平和线粒体膜电位方面的新鲜卵母细胞。总之，在玻璃化卵母细胞中的高偏振线粒体分布的改变可能对线粒体活性产生影响，包括在受精期间的ROS产生和进一步发展。在未成熟的玻璃化/升温卵母细胞的体外成熟之前，在体外成熟之前预孵育可能有助于再分布高偏振线粒体内膜电位和减少ROS并在受精后提高进一步的胚胎发育。

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