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Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury.
Brain Res. 2009 Aug 04; 1283:139-47.BR

Abstract

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.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Wang H
Department of Neurobiology, State Key Laboratory of Medical Neurobiology, Shanghai Medical College, Fudan University, Shanghai 200032, PR China.
Xu Y
No affiliation info available
Yan J
No affiliation info available
Zhao X
No affiliation info available
Sun X
No affiliation info available
Zhang Y
No affiliation info available
Guo J
No affiliation info available
Zhu C
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAntioxidantsApoptosisApoptosis Regulatory ProteinsCaspase 3Cell Line, TumorCell SurvivalCytochromes cGlucosidesHumansMembrane Potential, MitochondrialNerve DegenerationNeuronsNeuroprotective AgentsOxidative StressPeptide FragmentsPhenolsProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19520063

Citation

Wang, Hongquan, et al. "Acteoside Protects Human Neuroblastoma SH-SY5Y Cells Against Beta-amyloid-induced Cell Injury." Brain Research, vol. 1283, 2009, pp. 139-47.
Wang H, Xu Y, Yan J, et al. Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury. Brain Res. 2009;1283:139-47.
Wang, H., Xu, Y., Yan, J., Zhao, X., Sun, X., Zhang, Y., Guo, J., & Zhu, C. (2009). Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury. Brain Research, 1283, 139-47. https://doi.org/10.1016/j.brainres.2009.05.101
Wang H, et al. Acteoside Protects Human Neuroblastoma SH-SY5Y Cells Against Beta-amyloid-induced Cell Injury. Brain Res. 2009 Aug 4;1283:139-47. PubMed PMID: 19520063.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury. AU - Wang,Hongquan, AU - Xu,Yuxia, AU - Yan,Jie, AU - Zhao,Xiaoyan, AU - Sun,Xiaobo, AU - Zhang,Yanping, AU - Guo,Jingchun, AU - Zhu,Cuiqing, Y1 - 2009/06/09/ PY - 2009/04/27/received PY - 2009/05/24/revised PY - 2009/05/27/accepted PY - 2009/6/13/entrez PY - 2009/6/13/pubmed PY - 2009/10/24/medline SP - 139 EP - 47 JF - Brain research JO - Brain Res VL - 1283 N2 - 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. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/19520063/Acteoside_protects_human_neuroblastoma_SH_SY5Y_cells_against_beta_amyloid_induced_cell_injury_ DB - PRIME DP - Unbound Medicine ER -