Abstract Title:

Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury.

Abstract Source:

Brain Res. 2009 Aug 4 ;1283:139-47. Epub 2009 Jun 9. PMID: 19520063

Abstract Author(s):

Hongquan Wang, Yuxia Xu, Jie Yan, Xiaoyan Zhao, Xiaobo Sun, Yanping Zhang, Jingchun Guo, Cuiqing Zhu

Article Affiliation:

Hongquan Wang


Amyloid beta-peptide (Abeta) has been implicated in the pathogenesis of AD. It can cause cell death in AD by evoking a cascade of oxidative damage to neurons. So antioxidant compounds may throw a light on the treatment of AD. In the present study, we investigated the protective effect of acteoside (AS), an antioxidative phenylethanoid glycoside, on Abeta(25-35)-induced SH-SY5Y cell injury. Exposure of cells to 25 muM Abeta(25-35) for 24 h caused viability loss, apoptotic increase and reactive oxygen species (ROS) increase, pre-treatment with acteoside for 1.5 h significantly reduced the viability loss, apoptotic rate and attenuated Abeta-mediated ROS production. In addition, AS strikingly inhibited Abeta(25-35)-induced mitochondrial dysfunctions, including lowered membrane potential, increased Bax/Bcl-2 ratio, cytochrome c release and the cleavage of caspase-3. Taken together, these results indicated that acteoside could protect SH-SY5Y cells against beta-amyloid-induced cell injury by the attenuating ROS production and the modulating apoptotic signal pathway through Bcl-2 family, cytochrome c, and caspase-3.

Study Type : In Vitro Study

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