4.5 Article

Insulin-like growth factor-1 protects SH-SY5Y cells against β-amyloid-induced apoptosis via the PI3K/Akt-Nrf2 pathway

期刊

EXPERIMENTAL GERONTOLOGY
卷 87, 期 -, 页码 23-32

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2016.11.009

关键词

IGF-1; beta-amyloid; Apoptosis; Oxidative stress; PI3K/Akt; Nrf2

资金

  1. Jinshan Municipal Population and Family Planning Commission [JSKJ-KTQN-2014-08]
  2. Science and Technology Commission of Shanghai Municipality [20164Y0193]

向作者/读者索取更多资源

Insulin-like growth factor-1 (IGF-1) shows protective effect against A beta-induced cytotoxicity and apoptosis, but the underlying mechanisms are poorly characterized. The present study was conducted to explore the mechanisms involved in the beneficial effect of IGF-1 against A beta-induced apoptosis in SH-SY5Y cells. We found that pretreatment with IGF-1 attenuated A beta(25-35)-induced loss of cell viability and apoptosis in SH-SY5Y cells in a dose dependent manner. In addition, IGF-1 inhibited the generation of reactive oxygen species (ROS) and increased the antioxidant activity in A beta(25-35)-treated cells. Further, IGF-1 significantly promoted the nuclear translocation of Nrf2, and upregulated the expression of its downstream gene heme oxygenase-1 (HO-1). Moreover, LY294002, a specific PI3K inhibitor, was found to completely abolish the protective effect of IGF-1 on A beta(25-35)-induced apoptosis and ROS generation. Together, our findings suggest that IGF-1 protects SH-SY5Y cells against A beta(25-35)-induced cell injury by scavenging ROS via the PI3K/Akt-Nrf2 signaling pathway. (C) 2016 Published by Elsevier Inc.

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