OALib Journal期刊
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beclin1在长春新碱致斑马鱼多巴胺能神经元损伤中的作用
, PP. 843-848
Keywords: 长春新碱,自噬,凋亡,beclin1,多巴胺能神经元
Abstract:
以斑马鱼幼鱼为实验动物,通过rt-pcr、westernblotting、过表达、knockdown和整体免疫荧光等技术手段,研究长春新碱导致的斑马鱼幼鱼多巴胺能神经元损伤的分子机制,并探索降低长春新碱毒性的分子靶标。结果显示,长春新碱抑制多巴胺能神经元标志基因酪氨酸羟化酶基因、多巴胺转运蛋白基因转录水平,诱导幼鱼脑部多巴胺能神经元细胞丢失。长春新碱浓度依赖性抑制自噬相关基因beclin1的表达,过表达beclin1基因对长春新碱诱导的多巴胺能神经元毒性具有挽救作用,下调beclin1基因加剧长春新碱导致的多巴胺能神经元细胞毒性。结果提示,beclin1基因可能在长春新碱导致的神经毒性中发挥重要作用。
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