Dalian Key Laboratory of Hematology; Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, Dalian, Liaoning, China.
Department of Occupational and Environmental Health, School of Public Health, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Adv Exp Med Biol. 2019;1155:949-958. doi: 10.1007/978-981-13-8023-5_79.
Taurine is an important amino acid for the growth and development of the central nervous system and plays an important role in the development of the nervous system. Many studies have shown that taurine can prevent and repair neurodevelopmental damage, and its mechanism has also become a research hotspot. While most studies focus on nerve cells, less on placental cells that are closely related to early neurodevelopment (developmental neurotoxicity) by modulating fetal circulation level of thyroid hormones. Studies have shown that exposure of placental cells to the common environmental endocrine disruptor BDE 209 during early pregnancy may lead to developmental neurotoxicity due to thyroid hormone interference caused by abnormal expression of deiodinases. Therefore, in this study, the placenta-derived JEG cells cultured at 95% air/5% CO2 was used as a in vitro model, and the potential protection from taurine on BDE 209-mediated cytotoxicity was examined. When BDE 209 was found to cause a decrease in cell viability and disturbance in the gene and protein expressions of placental deiodinase 3, pretreatment of the JEG cells with taurine can moderately reduce the BDE 209-meditated cytotoxicity, and restore gene and protein expressions of placental deiodinase, so that thyroid hormone levels tend to be normal in cell culture medium. Our data suggest that taurine may have some protection on the developmental neurotoxicity caused by BDE 209.
牛磺酸是中枢神经系统生长发育的重要氨基酸,在神经系统发育中发挥重要作用。许多研究表明,牛磺酸可以预防和修复神经发育损伤,其机制也成为研究热点。虽然大多数研究都集中在神经细胞上,但对于与早期神经发育(发育神经毒性)密切相关的胎盘细胞关注较少,通过调节胎儿循环中甲状腺激素的水平。研究表明,妊娠早期胎盘细胞暴露于常见的环境内分泌干扰物 BDE 209 可能会因脱碘酶表达异常导致甲状腺激素干扰而导致发育神经毒性。因此,在这项研究中,使用胎盘来源的 JEG 细胞在 95%空气/5% CO2 下培养作为体外模型,研究了牛磺酸对 BDE 209 介导的细胞毒性的潜在保护作用。当发现 BDE 209 导致细胞活力下降和胎盘脱碘酶 3 的基因和蛋白表达紊乱时,JEG 细胞用牛磺酸预处理可以适度减轻 BDE 209 介导的细胞毒性,并恢复胎盘脱碘酶的基因和蛋白表达,使细胞培养液中的甲状腺激素水平趋于正常。我们的数据表明,牛磺酸可能对 BDE 209 引起的发育神经毒性具有一定的保护作用。