title: Protective effect of paeoniflorin on Aβ25-35-induced SH-SY5Y cell injury by preventing mitochondrial dysfunction.
abstract: Alzheimer's disease (AD) is a major neurodegenerative brain disorder affecting about 14 million people worldwide. Aβ-induced cell injury is a crucial cause of neuronal loss in AD, thus the suppression of which might be useful for the treatment of this disease. In this study, we aimed to evaluate the effect of paeoniflorin (PF), a monoterpene glycoside isolated from aqueous extract of Radix Paeoniae Alba, on Aβ25-35-induced cytotoxicity in SH-SY5Y cells. The results showed PF could attenuate or restore the viability loss, apoptotic increase, and ROS production induced by Aβ25-35 in SH-SY5Y cells. In addition, PF strikingly inhibited Aβ25-35-induced mitochondrial dysfunction, which includes decreased mitochondrial membrane potential, increased Bax/Bcl-2 ratio, cytochrome c release and activity of caspase-3 and caspase-9. Therefore, our study provided the first experimental evidence that PF could modulate ROS production and apoptotic mitochondrial pathway in model of neuron injury in vitro and which might provide new insights into its application toward Alzheimer's disease therapy.
authors.affiliation: Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, 214063, Jiangsu Province, China, nypd0723@gmail.com.
authors.forename: Ke
authors.initials: K
authors.lastname: Wang
authors.forename: Ling
authors.initials: L
authors.lastname: Zhu
authors.forename: Xue
authors.initials: X
authors.lastname: Zhu
authors.forename: Kai
authors.initials: K
authors.lastname: Zhang
authors.forename: Biao
authors.initials: B
authors.lastname: Huang
authors.forename: Jue
authors.initials: J
authors.lastname: Zhang
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.forename: Lan
authors.initials: L
authors.lastname: Zhu
authors.forename: Bin
authors.initials: B
authors.lastname: Zhou
authors.forename: Fanfan
authors.initials: F
authors.lastname: Zhou
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity*; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D005960:Glucosides / Q000494:pharmacology*; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D039821:Monoterpenes / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments / Q000633:toxicity*; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D006027:Glycosides
chemical_list: D016229:Amyloid beta-Peptides; D053148:Caspase 3; D053453:Caspase 9; D045304:Cytochromes c; D005960:Glucosides; D039821:Monoterpenes; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D051028:bcl-2-Associated X Protein; C074636:amyloid beta-protein (25-35); C015423:peoniflorin; D006027:Glycosides