IGF-1/AKT信号减弱了诱导的神经细胞亡和DNA碎片化的作用
1School of Pharmacy, Faculty of Health & Medical Sciences, Taylor's University, Subang Jaya, Malaysia.
概括
胰岛素样生长因子-1 (IGF-1) 通过重新激活PI3K/AKT通路来防止引起的神经毒性. 这项研究表明,IGF-1减少神经元亡和DNA碎片化,为中毒提供了潜在的治疗标.
科学领域:
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
背景情况:
- 长期暴露于会导致神经毒性,氧化应激和亡.
- 对引起的神经毒性的保护策略是有限的.
- 胰岛素样生长因子-1 (IGF-1) 对神经毒性的神经保护潜力在很大程度上尚未被探索.
研究的目的:
- 研究IGF-1在人类SH-SY5Y神经母细胞瘤细胞中对酸 (NaAsO2) 诱导的神经毒性的神经保护作用.
- 阐明涉及IGF-1/AKT信号通路和亡调节的潜在分子机制.
主要方法:
- 人类SH-SY5Y神经母细胞瘤细胞 (分化和不分化) 暴露于NaAsO2与或没有IGF-1治疗.
- 西方涂抹被用于评估AKT酸化.
- 通过流细胞计和免疫阻塞检测apoptotic标记物 (caspase-3, PARP, p53, Bcl-2) 来评估亡和DNA碎片化.
主要成果:
- 暴露于NaAsO2抑制了AKT酸化,并诱导了度依赖的亡,增加了p53,分裂的caspase-3和PARP裂变.
- IGF-1治疗显著减轻了NaAsO2诱导的亡和DNA分裂.
- IGF-1恢复了AKT信号传递,减少了亲细胞亡标记物,并减少了细胞亡细胞死亡.
结论:
- 通过重新激活PI3K/AKT通路,IGF-1可以保护诱导的神经亡和DNA碎片化.
- 这种重新激活会重新平衡apoptotic调节器并抑制p53-介导的亡.
- IGF-1信号传递代表了与有关的神经元损伤的有前途的治疗标.
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