Abstract：
This study was designed to investigate the potential neuronal damage mechanism of the okadaic acid (OA) in the brain tissues of zebrafish embryos by evaluating in terms of immunofluorescence of Nf KB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG signaling pathways. We also evaluated body malformations. For this purpose, zebrafish embryos were exposed to 0.5 μg/ml, 1 μg/ml and 2.5 μg/ml of OA for 5 days. After application, FITC/GFP labeled protein-specific antibodies were used in immunofluorescence assay for NfKB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG respectively. The results indicated that OA caused immunofluorescence positivity of NfKB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG in a dose-dependent manner in the brain tissues of zebrafish embryos. Pericardial edema (PE), nutrient sac edema (YSE) and body malformations, tail malformation, short tail and head malformation (BM) were detected in zebrafish embryos. These results suggest that OA induces neuronal damage by affecting the modulation of DNA damage, apoptotic, and inflammatory activities in the brain tissues of zebrafish embryos. The increase in signaling pathways shows that OA can cause damage in the structure and function of brain nerve cells. Our results provide a new basis for the comprehensive assessment of the neural damage of OA and will offer enable us to better understand molecular the mechanisms underlying the pathophysiology of OA toxicity.
摘要：
本研究旨在通过对NfKB的免疫荧光评估，探讨斑马鱼胚胎脑组织中冈田酸（OA）的潜在神经元损伤机制。TLR-4，胱天蛋白酶3，ERK½，c-FOS和8-OHdG信号通路。我们还评估了身体畸形。为此,斑马鱼胚胎暴露于0.5μg/ml，1μg/ml和2.5μg/ml的OA持续5天。申请后,FITC/GFP标记的蛋白质特异性抗体用于NfKB的免疫荧光测定，TLR-4，胱天蛋白酶3，ERK½，c-FOS和8-OHdG。结果表明，OA引起NfKB的免疫荧光阳性，TLR-4，胱天蛋白酶3，ERK½，斑马鱼胚胎脑组织中的c-FOS和8-OHdG呈剂量依赖性。心包水肿(PE),营养囊水肿（YSE）和身体畸形，尾巴畸形,在斑马鱼胚胎中检测到短尾和头部畸形（BM）。这些结果表明，OA通过影响DNA损伤的调节来诱导神经元损伤，凋亡，斑马鱼胚胎脑组织中的炎症活动。信号通路的增加表明OA可引起脑神经细胞结构和功能的损害。我们的结果为全面评估OA的神经损伤提供了新的基础，并将使我们更好地了解OA毒性病理生理学的分子机制。
