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首页> 外文期刊>Czech Journal of Animal Science >Inhibition of c-Jun N-terminal kinase (JNK) suppresses porcine oocyte ageing in vitro
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Inhibition of c-Jun N-terminal kinase (JNK) suppresses porcine oocyte ageing in vitro

机译：抑制c-Jun N端激酶（JNK）体外抑制猪卵母细胞衰老

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摘要

Oocyte ageing is a complex of processes that occur when matured in vitro oocytes are, after reaching the metaphase ii stage, exposed to further in vitro culture. Aged oocytes remaining at the metaphase ii stage undergo spontaneous parthenogenetic activation, or cellular death, through apoptosis (fragmentation) or lysis. The key factor in apoptotic pathway regulation is c-Jun-N-terminal kinase (JNK), stress kinase from the mitogene-activated protein kinase (MAPK) family. To investigate the effect of JNK inhibition on porcine oocytes ageing, cleavage rate, and embryonic development after parthenogenetic activation, DNA fragmentation, and pro-apoptotic factor Bax expression, we cultured in vitro matured oocytes for another 1-4 days in the presence of aJNK inhibitor. The inhibition of JNK significantiy protected the oocytes from fragmentation (0% of fragmented oocytes under JNK inhibition vs. 13.4% of fragmented oocytes in the control group, 2nd day of ageing) and increased the percentage of parthenogenetically activated oocytes (82 vs 57.7%, 2nd day of ageing). The embryonic development of oocytes parthenogenetically activated after 24 h of ageing was influenced by JNK inhibition as well. The percentage of oocytes at the morula stage, after seven days of cultivation, was significantly increased when oocytes aged in the presence of a JNK inhibitor (42.5%) by comparison to the percentage of oocytes exposed to ageing in an inhibitor-free medium (23.3%). DNA fragmentation was significantly suppressed by JNK inhibition from the 1st day of ageing, but the expression of pro-apoptotic factor Bax in the oocytes was not influenced. On the basis of our experiments, we can conclude that JNK inhibition suppresses apoptosis and DNA fragmentation of aged oocytesand improves their embryonic development following the parthenogenetic activation. However, to completely eliminate all ageing related processes is insufficient.
机译：卵母细胞衰老是过程的复杂过程，当成熟的体外卵母细胞达到中期ii期后，再进行进一步的体外培养时，就会发生这些过程。保留在中期ii期的老化卵母细胞通过凋亡（片段化）或裂解而经历自发的孤雌生殖活化或细胞死亡。凋亡途径调控的关键因素是c-Jun-N-末端激酶（JNK），这是一种来自基因表达激活的蛋白激酶（MAPK）家族的应激激酶。为了研究JNK抑制对孤雌遗传激活，DNA片段化和促凋亡因子Bax表达后猪卵母细胞老化，卵裂率和胚胎发育的影响，我们在存在aJNK的情况下将体外成熟的卵母细胞再培养1-4天抑制剂。抑制JNK可以显着保护卵母细胞免于破碎（在老化第2天，对照组中0％的卵母细胞比对照组的13.4％的卵母细胞破碎），并且增加了孤雌性激活的卵母细胞的百分比（82对57.7％，老化的第二天）。老化24小时后被孤雌性​​激活的卵母细胞的胚胎发育也受到JNK抑制的影响。与在无抑制剂培养基中暴露于老化的卵母细胞的百分比相比（23.3），当在JNK抑制剂存在下老化的卵母细胞（42.5％）老化后，经过7天的培养，桑stage期卵母细胞的百分比显着增加。 ％）。从衰老的第一天起，JNK抑制作用就显着抑制了DNA片段化，但是卵母细胞中促凋亡因子Bax的表达没有受到影响。根据我们的实验，我们可以得出结论，JNK抑制抑制衰老卵母细胞的凋亡和DNA片段化，并改善孤雌生殖激活后它们的胚胎发育。但是，完全消除所有与老化相关的过程是不够的。

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