title: Acteoside protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury.
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.
authors.affiliation: Department of Neurobiology, State Key Laboratory of Medical Neurobiology, Shanghai Medical College, Fudan University, Shanghai 200032, PR China.
authors.forename: Hongquan
authors.initials: H
authors.lastname: Wang
authors.forename: Yuxia
authors.initials: Y
authors.lastname: Xu
authors.forename: Jie
authors.initials: J
authors.lastname: Yan
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Zhao
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Sun
authors.forename: Yanping
authors.initials: Y
authors.lastname: Zhang
authors.forename: Jingchun
authors.initials: J
authors.lastname: Guo
authors.forename: Cuiqing
authors.initials: C
authors.lastname: Zhu
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000633:toxicity; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D051017:Apoptosis Regulatory Proteins / Q000187:drug effects / Q000378:metabolism; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D045304:Cytochromes c / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects / Q000502:physiology; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D010446:Peptide Fragments / Q000037:antagonists & inhibitors / Q000633:toxicity; D010636:Phenols / Q000494:pharmacology* / Q000627:therapeutic use; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D059808:Polyphenols
chemical_list: D016229:Amyloid beta-Peptides; D000975:Antioxidants; D051017:Apoptosis Regulatory Proteins; D053148:Caspase 3; D045304:Cytochromes c; D005960:Glucosides; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D010636:Phenols; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; C074636:amyloid beta-protein (25-35); C058956:acteoside; D059808:Polyphenols