胚胎暴露于德巴因会诱导斑马鱼发育中的多重神经管缺陷
Venugopalan Rajesh1, Pachangattupalayam Karuppusamy Divya2
1Department of Pharmacology, The Erode College of Pharmacy and Research Institute affiliated to The Tamil Nadu Dr. M.G.R. Medical University, Veppampalayam, Vallipurathampalayam (Po), Erode, Chennai, Tamil Nadu, 638112, India. rajesh.v@ecp.ac.in.
Fish physiology and biochemistry
|November 20, 2023
概括
在斑马鱼胚胎发育过程中暴露于德西塔,导致显著的神经管缺陷. 这突显了DNA甲基化在预防这些严重的先天性疾病中的关键作用.
科学领域:
- 发育生物学是发展生物学.
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 毒理学 毒理学 毒理学
背景情况:
- 神经管缺陷 (NTDs) 是一种严重的先天性疾病,每1000例新生儿中会发生1-2例.
- 多因素病因涉及遗传和环境因素.
- 表观遗传失调,特别是异常的DNA甲基化,与NTD有关.
研究的目的:
- 调查DNA甲基化抑制剂基 (DCT) 对斑马鱼胚胎神经管形成的影响.
- 评估度依赖的德西他对胚胎发育和NTD的影响.
主要方法:
- 在神经分泌之前,斑马鱼胚胎被暴露在不同度的迪西塔宾 (13.69微米至1毫米) 中.
- 监测了发育,并在受精后120小时评估了NTD.
- 阿利扎林红色染色和组织病理学检查了神经管和体内形态.
主要成果:
- 暴露于decitabine导致神经管和体内细胞发育的异常,并延迟了化.
- 观察到NTD患病率和严重程度的度依赖的增加.
- 高度的迪西他 (1毫米) 导致广泛的发育不良,90%的人表现出多种NTD.
结论:
- 德西塔显著损害斑马鱼的神经管发育.
- 研究结果支持这样一个假设:胚胎发生过程中的低甲基化是神经管缺陷的原因.
- 这项研究强调了DNA甲基化抑制剂对胚胎发育的有害影响.
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