Prenatal hyperhomocysteinemia (PHHC) in pregnant rats was induced by chronic L-methionine loading, resulting in a significant increase in the L-homocysteine content both in the mothers’ blood and blood and brain of fetuses. Significant decrease in the weight of the placenta, fetus, and fetal brain was detected by the morphometric studies on day 20 of pregnancy. PHHC also activated maternal immune system due to the increase in the content of proinflammatory inter-leukin-1β in the rat blood and fetal part of the placenta. PHHC elevated the levels of the brain-derived neurotrophic factor (BDNF, 29 kDa) and nerve growth factor (NGF, 31 kDa) precursors in the placenta and the content of the BDNF isoform (29 kDa) in the fetal brain. The content of neuregulin 1 (NRG1) decreased in the placenta and increased in the fetal brain on day 20 of embryonic development. An increase in the caspase-3 activity was detected in the brains of fetuses subjected to PHHC. It was suggested that changes in the processing of neurotrophins induced by PPHC, oxidative stress, and inflammatory processes initiated by it, as well as apoptosis, play an important role in the development of brain disorders in the offspring.

中文翻译：

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产前高同型半胱氨酸血症中胎儿脑和胎盘的神经营养因子

妊娠大鼠的产前高同型半胱氨酸血症 (PHHC) 是由慢性 L-甲硫氨酸负荷引起的，导致母亲血液和胎儿血液和大脑中 L-同型半胱氨酸含量显着增加。妊娠第 20 天的形态计量学研究检测到胎盘、胎儿和胎儿大脑的重量显着下降。由于大鼠血液和胎盘胎儿部分中促炎性白细胞介素 1β 含量的增加，PHHC 还激活了母体免疫系统。PHHC 提高了胎盘中脑源性神经营养因子 (BDNF, 29 kDa) 和神经生长因子 (NGF, 31 kDa) 前体的水平以及胎儿大脑中 BDNF 同种型 (29 kDa) 的含量。在胚胎发育的第 20 天，胎盘中神经调节蛋白 1 (NRG1) 的含量减少，而在胎儿大脑中的含量增加。在接受 PHHC 的胎儿的大脑中检测到 caspase-3 活性的增加。有人提出，由 PPHC 诱导的神经营养因子处理的变化、氧化应激和由其引发的炎症过程以及细胞凋亡，在后代脑部疾病的发展中起着重要作用。